タムラ キヨミ田村 潔美教授Kiyomi Tamura
■研究者基本情報
経歴
■研究活動情報
受賞
論文
- Pharmacological control of angiogenesis by regulating phosphorylation of myosin light chain 2
Kiyomi Tsuji-Tamura; Mari Sato; Masato Tamura, 筆頭著者, Background
Control of angiogenesis is widely considered a therapeutic strategy, but reliable control methods are still under development. Phosphorylation of myosin light chain 2 (MLC2), which regulates actin-myosin interaction, is critical to the behavior of vascular endothelial cells (ECs) during angiogenesis. MLC2 is phosphorylated by MLC kinase (MLCK) and dephosphorylated by MLC phosphatase (MLCP) containing a catalytic subunit PP1. We investigated the potential role of MLC2 in the pharmacological control of angiogenesis.
Methods and results
We exposed transgenic zebrafish Tg(fli1a:Myr-mCherry)ncv1 embryos to chemical inhibitors and observed vascular development. PP1 inhibition by tautomycetin increased length of intersegmental vessels (ISVs), whereas MLCK inhibition by ML7 decreased it; these effects were not accompanied by structural dysplasia. ROCK inhibition by Y-27632 also decreased vessel length. An in vitro angiogenesis model of human umbilical vein endothelial cells (HUVECs) showed that tautomycetin increased vascular cord formation, whereas ML7 and Y-27632 decreased it. These effects appear to be influenced by regulation of cell morphology rather than cell viability or motility. Actin co-localized with phosphorylated MLC2 (pMLC2) was abundant in vascular-like elongated-shaped ECs, but poor in non-elongated ECs. pMLC2 was associated with tightly arranged actin, but not with loosely arranged actin. Moreover, knockdown of MYL9 gene encoding MLC2 reduced total MLC2 and pMLC2 protein and inhibited angiogenesis in HUVECs.
Conclusion
The present study found that MLC2 is a pivotal regulator of angiogenesis. MLC2 phosphorylation may be involved in the regulation of of cell morphogenesis and cell elongation. The functionally opposite inhibitors positively or negatively control angiogenesis, probably through the regulating EC morphology. These findings may provide a unique therapeutic target for angiogenesis.
Cellular signalling, 2024年08月, ［査読有り］ - FOXO1 promotes endothelial cell elongation and angiogenesis by up-regulating the phosphorylation of myosin light chain 2
Kiyomi Tsuji-Tamura; Minetaro Ogawa, 筆頭著者, The forkhead box O1 (FOXO1) is an important transcription factor related to proliferation, metabolism, and homeostasis,
while the major phenotype of FOXO1-null mice is abnormal vascular morphology, such as vessel enlargement and dilation.
In in vitro mouse embryonic stem cell (ESC)-differentiation system, Foxo1−/− vascular endothelial cells (ECs) fail to elongate,
and mimic the abnormalities of FOXO1-deficiency in vivo. Here, we identified the PPP1R14C gene as the FOXO1 target
genes responsible for elongating using transcriptome analyses in ESC-derived ECs (ESC-ECs), and found that the FOXO1-
PPP1R14C-myosin light chain 2 (MLC2) axis is required for EC elongation during angiogenesis. MLC2 is phosphorylated by
MLC kinase (MLCK) and dephosphorylated by MLC phosphatase (MLCP). PPP1R14C is an inhibitor of PP1, the catalytic
subunit of MLCP. The abnormal morphology of Foxo1−/− ESC-ECs was associated with low level of PPP1R14C and loss
of MLC2 phosphorylation, which were reversed by PPP1R14C-introduction. Knockdown of either FOXO1 or PPP1R14C
suppressed vascular cord formation and reduced MLC2 phosphorylation in human ECs (HUVECs). The mouse and human
PPP1R14C locus possesses an enhancer element containing conserved FOXO1-binding motifs. In vivo chemical inhibition
of MLC2 phosphorylation caused dilated vascular structures in mouse embryos. Furthermore, foxo1 or ppp1r14c-knockdown
zebrafish exhibited vascular malformations, which were also restored by PPP1R14C-introduction. Mechanistically, FOXO1
suppressed MLCP activity by up-regulating PPP1R14C expression, thereby promoting MLC2 phosphorylation and EC elongation, which are necessary for vascular development. Given the importance of MLC2 phosphorylation in cell morpho-genesis, this study may provide novel insights into the role of FOXO1 in control of angiogenesis., Springer Science and Business Media LLC
Angiogenesis, 2023年11月, ［査読有り］ - Basic fibroblast growth factor uniquely stimulates quiescent vascular smooth muscle cells and induces proliferation and dedifferentiation.
Kiyomi Tsuji-Tamura; Masato Tamura, 筆頭著者, Blood vessels normally remain stable over the long term. However, in atherosclerosis, vascular cells leave the quiescent state and enter an activated state. Here, we investigated the factors that trigger the breakage of the quiescent state by screening growth factors and cytokines using a vascular smooth muscle cell (SMC) line and an endothelial cell (EC) line. Despite known functions of the tested factors, only basic fibroblast growth factor (bFGF) was identified as a potent trigger of quiescence breakage in SMCs, but not ECs. bFGF disrupted tight SMC-monolayers and caused morphological changes, proliferation, and dedifferentiation. Human primary SMCs, but not ECs, also showed similar results. Aberrant SMC proliferation is a critical histological event in atherosclerosis. We, thus, provide further insights into the role of bFGF in vascular pathobiology.
FEBS letters, 2022年07月, ［査読有り］ - The canonical smooth muscle cell marker TAGLN is present in endothelial cells and is involved in angiogenesis
Kiyomi Tsuji-Tamura; Saori Morino-Koga; Shingo Suzuki; Minetaro Ogawa, 筆頭著者, Elongation of vascular endothelial cells (ECs) is an important process in angiogenesis; however, the molecular mechanisms remain unknown. The actin-crosslinking protein TAGLN (transgelin, also known as SM22 or SM22α) is abundantly expressed in smooth muscle cells (SMCs) and is widely used as a canonical marker for this cell type. In the course of studies using mouse embryonic stem cells (ESCs) carrying an Tagln promoter-driven fluorescence marker, we noticed activation of the Tagln promoter during EC elongation. Tagln promoter activation co-occurred with EC elongation in response to vascular endothelial growth factor A (VEGF-A). Inhibition of phosphoinositide 3-kinase (PI3K)-Akt signaling and mTORC1 also induced EC elongation and Tagln promoter activation. Human umbilical vein endothelial cells (HUVECs) elongated, activated the TAGLN promoter and increased TAGLN transcripts in an angiogenesis model. Genetic disruption of TAGLN augmented angiogenic behaviors of HUVECs, as did the disruption of TAGLN2 and TAGLN3 genes. Tagln expression was found in ECs in mouse embryos. Our results identify TAGLN as a putative regulator of angiogenesis whose expression is activated in elongating ECs. This finding provides insight into the cytoskeletal regulation of EC elongation and an improved understanding of the molecular mechanisms underlying the regulation of angiogenesis.
Journal of cell science, 2021年08月02日, ［査読有り］ - Osteocytes as main responders to low-intensity pulsed ultrasound treatment during fracture healing.
Tatsuya Shimizu; Naomasa Fujita; Kiyomi Tsuji-Tamura; Yoshimasa Kitagawa; Toshiaki Fujisawa; Masato Tamura; Mari Sato, Ultrasound stimulation is a type of mechanical stress, and low-intensity pulsed ultrasound (LIPUS) devices have been used clinically to promote fracture healing. However, it remains unclear which skeletal cells, in particular osteocytes or osteoblasts, primarily respond to LIPUS stimulation and how they contribute to fracture healing. To examine this, we utilized medaka, whose bone lacks osteocytes, and zebrafish, whose bone has osteocytes, as in vivo models. Fracture healing was accelerated by ultrasound stimulation in zebrafish, but not in medaka. To examine the molecular events induced by LIPUS stimulation in osteocytes, we performed RNA sequencing of a murine osteocytic cell line exposed to LIPUS. 179 genes reacted to LIPUS stimulation, and functional cluster analysis identified among them several molecular signatures related to immunity, secretion, and transcription. Notably, most of the isolated transcription-related genes were also modulated by LIPUS in vivo in zebrafish. However, expression levels of early growth response protein 1 and 2 (Egr1, 2), JunB, forkhead box Q1 (FoxQ1), and nuclear factor of activated T cells c1 (NFATc1) were not altered by LIPUS in medaka, suggesting that these genes are key transcriptional regulators of LIPUS-dependent fracture healing via osteocytes. We therefore show that bone-embedded osteocytes are necessary for LIPUS-induced promotion of fracture healing via transcriptional control of target genes, which presumably activates neighboring cells involved in fracture healing processes.
Scientific reports, 2021年05月13日, ［査読有り］ - The role of PI3K/Akt/mTOR signaling in dose-dependent biphasic effects of glycine on vascular development.
Kiyomi Tsuji-Tamura; Mari Sato; Misato Fujita; Masato Tamura, 筆頭著者, Glycine, a non-essential amino acid, exerts concentration-dependent biphasic effects on angiogenesis. Low-doses of glycine promote angiogenesis, whereas high-doses cause anti-angiogenesis. The phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling participates in angiogenesis of both physiological development, and pathological events including tumor and inflammation. We assessed the role of PI3K/Akt/mTOR signaling in vascular development, and the interaction with glycine, using transgenic zebrafish Tg(fli1a:Myr-mCherry)ncv1 embryos expressing fluorescent proteins in vascular endothelial cells. Treatment with inhibitors of mTORC1 (rapamycin and everolimus), mTORC1/mTORC2 (KU0063794), PI3K (LY29400), and Akt (Akt inhibitor) decreased the development of intersegmental vessels (ISVs). These inhibitors cancelled the angiogenic effects of a low-dose of glycine, while acted synergistically with a high-dose of glycine in anti-angiogenesis. mTOR signaling regulates the gene expression of vascular endothelial growth factor (VEGF), a major angiogenic factor, and nitric oxide (NO) synthase (NOS), an enzyme for the synthesis of an angiogenic mediator NO. Expressions of VEGF and NOS were consistent with the vascular features induced by glycine and an mTOR inhibitor. Our results suggest that PI3K/Akt/mTOR signaling may interact with dose-dependent biphasic effects of exogenous glycine on in vivo angiogenesis. mTOR signaling is a key target for cancer therapy, thus, the combining mTOR inhibitors with glycine may be a potential approach for controlling angiogenesis.
Biochemical and biophysical research communications, 2020年08月27日, ［査読有り］ - Glycine exerts dose-dependent biphasic effects on vascular development of zebrafish embryos.
Kiyomi Tsuji-Tamura; Mari Sato; Misato Fujita; Masato Tamura, 筆頭著者, Glycine, a non-essential amino acid, is involved in both angiogenesis and anti-angiogenesis. We hypothesized that glycine would exert dose-dependent different effects on angiogenesis. In this study, we investigated the effects of a broad range of concentrations of glycine on vascular development using transgenic zebrafish Tg(fli1a:Myr-mCherry)ncv1 embryos. Effects of glycine transporter (GlyT) inhibitors (sarcosine and bitopertin) and a glycine receptor (GlyR) inhibitor (strychnine) were also examined in embryos in the absence or presence of glycine. After exposure to glycine and inhibitors, intersegmental vessels (ISVs) were observed by fluorescent microscopy. Low concentrations of glycine promoted the development of ISVs, whereas high concentrations reduced it. These effects of glycine could generally be reversed by treatment with GlyT and GlyR inhibitors. Furthermore, expressions of vascular endothelial growth factor (VEGF) (an angiogenic factor) and nitric oxide synthase (NOS) (an enzyme for nitric oxide synthesis) were associated with the dose-dependent effects of glycine. Our results suggest that glycine exerts dose-dependent biphasic effects on vascular development, which rely on GlyTs and GlyRs, and correlate with the expression of VEGF and NOS genes. At low concentrations, glycine acted as an angiogenic factor. In contrast, at high concentrations, glycine induced anti-angiogenesis. This evidence provides a novel insight into glycine as a unique target in angiogenic and anti-angiogenic therapy.
Biochemical and biophysical research communications, 2020年06月25日, ［査読有り］ - Morphology regulation in vascular endothelial cells.
Kiyomi Tsuji-Tamura; Minetaro Ogawa, 筆頭著者, Morphological change in endothelial cells is an initial and crucial step in the process of establishing a functional vascular network. Following or associated with differentiation and proliferation, endothelial cells elongate and assemble into linear cord-like vessels, subsequently forming a perfusable vascular tube. In vivo and in vitro studies have begun to outline the underlying genetic and signaling mechanisms behind endothelial cell morphology regulation. This review focuses on the transcription factors and signaling pathways regulating endothelial cell behavior, involved in morphology, during vascular development.
Inflammation and regeneration, 2018年09月10日, ［査読有り］, ［招待有り］ - Dual inhibition of mTORC1 and mTORC2 perturbs cytoskeletal organization and impairs endothelial cell elongation
Kiyomi Tsuji-Tamura; Minetaro Ogawa, 筆頭著者, Elongation of endothelial cells is an important process in vascular formation and is expected to be a therapeutic target for inhibiting tumor angiogenesis. We have previously demonstrated that inhibition of mTORC1 and mTORC2 impaired endothelial cell elongation, although the mechanism has not been well defined. In this study, we analyzed the effects of the mTORC1-specific inhibitor everolimus and the mTORC1/mTORC2 dual inhibitor KU0063794 on the cytoskeletal organization and morphology of endothelial cell lines. While both inhibitors equally inhibited cell proliferation, KU0063794 specifically caused abnormal accumulation of F-actin and disordered distribution of microtubules, thereby markedly impairing endothelial cell elongation and tube formation. The effects of KU0063794 were phenocopied by paclitaxel treatment, suggesting that KU0063794 might impair endothelial cell morphology through over-stabilization of microtubules. Although mTORC1 is a key signaling molecule in cell proliferation and has been considered a target for preventing angiogenesis, mTORC1 inhibitors have not been sufficient to suppress angiogenesis. Our results suggest that mTORC1/mTORC2 dual inhibition is more effective for anti-angiogenic therapy, as it impairs not only endothelial cell proliferation, but also endothelial cell elongation., Elsevier BV
Biochemical and Biophysical Research Communications, 2018年02月26日, ［査読有り］ - Vascular formation: in vitro differentiation of vascular endothelial cells from pluripotent stem cells
Kiyomi Tsuji-Tamura; Masato Tamura, 筆頭著者, During early vascular development, vascular endothelial cells (ECs) differentiate, proliferate, migrate, and change morphologically, forming tube-like vascular structures. The ECs are then surrounded by vascular smooth muscle cells (SMCs), leading to the formation of stable vascular structures, or vascular maturation. The stages of cell or tissue development can be monitored and analyzed using in vitro differentiation systems of pluripotent stem cells. In this review, we present the molecular mechanisms that regulate the developmental processes of vasculature.
Hokkaido Journal of Dental Science, 2017年09月15日 - 胚性幹細胞を用いた血管形成メカニズムの解明
田村-辻潔美; 田村正人, 筆頭著者, 血管形成は，血管内皮細胞が増殖・分化し，出芽・伸長・分岐・管腔形成といった複雑な形態変化を経て進行する．その後，血管内皮細胞の外側を血管壁細胞が取り囲むことで成熟した血管となる．胚性幹細胞（ES細胞）は，浮遊培養を行うと細胞が集合して胚様体と呼ばれる細胞凝集塊を形成する．この胚様体の中では，血管内皮細胞を含めた様々な種類の細胞分化や細胞間相互作用が起こる．そのため細胞・組織レベルでの発生過程のモデルとして解析されている ．OP9細胞は，マクロファージ刺激因子（M-CSF）に遺伝子異常を持つ骨大理石病マウス（op/opマウス）の新生仔の頭蓋冠から樹立されたストローマ細胞株であり，高い造血支持能を持つ．このOP9細胞をフィーダー細胞としてES細胞と共培養することで，血液細胞だけでなく血管細胞（血管内皮細胞，血管壁細胞）への効率的な分化誘導を行うことができる．また，タイプIVコラーゲンをコートしたプレートを用いることで，ES細胞から血管・血液細胞への無フィーダー培養系による分化誘導が可能である ．本稿では，血管細胞の増殖・分化と血管形成プロセスについて，ES細胞を用いた研究を中心に紹介する．, 北海道歯学会
北海道歯学雑誌, 2017年03月 - CXCR4 Signaling Negatively Modulates the Bipotential State of Hemogenic Endothelial Cells Derived from Embryonic Stem Cells by Attenuating the Endothelial Potential
Tanzir Ahmed; Kiyomi Tsuji-Tamura; Minetaro Ogawa, Hemogenic endothelial cells (HECs) are considered to be the origin of hematopoietic stem cells (HSCs). HECs have been identified in differentiating mouse embryonic stem cells (ESCs) as VE-cadherin+ cells with both hematopoietic and endothelial potential in single cells. Although the bipotential state of HECs is a key to cell fate decision toward HSCs, the molecular basis of the regulation of the bipotential state has not been well understood. Here, we report that the CD41+ fraction of CD45- CD31+ VE-cadherin+ endothelial cells (ECs) from mouse ESCs encompasses an enriched HEC population. The CD41+ ECs expressed Runx1, Tal1, Etv2, and Sox17, and contained progenitors for both ECs and hematopoietic cells (HCs) at a high frequency. Clonal analyses of cell differentiation confirmed that one out of five HC progenitors in the CD41+ ECs possessed the bipotential state that led also to EC colony formation. A phenotypically identical cell population was found in mouse embryos, although the potential was more biased to hematopoietic fate with rare bipotential progenitors. ESC-derived bipotential HECs were further enriched in the CD41+ CXCR4+ subpopulation. Stimulation with CXCL12 during the generation of VE-cadherin+ CXCR4+ cells attenuated the EC colony-forming ability, thereby resulted in a decrease of bipotential progenitors in the CD41+ CXCR4+ subpopulation. Our results suggest that CXCL12/CXCR4 signaling negatively modulates the bipotential state of HECs independently of the hematopoietic fate. Identification of signaling molecules controlling the bipotential state is crucial to modulate the HEC differentiation and to induce HSCs from ESCs., Oxford University Press (OUP)
Stem Cells, 2016年07月24日, ［査読有り］ - Inhibition of the PI3K–Akt and mTORC1 signaling pathways promotes the elongation of vascular endothelial cells
Kiyomi Tsuji-Tamura; Minetaro Ogawa, 筆頭著者, Endothelial cell morphology needs to be properly regulated during angiogenesis. Vascular endothelial growth factor (VEGF) induces endothelial cell elongation, which promotes sprouting of pre-existing vessels. However, therapeutic angiogenesis using VEGF has been hampered by side effects such as elevated vascular permeability. Here, we attempted to induce endothelial cell elongation without an overdose of VEGF. By screening a library of chemical inhibitors, we identified phosphatidylinositol 3-kinase (PI3K)-Akt pathway inhibitors and mammalian target of rapamycin complex 1 (mTORC1) inhibitors as potent inducers of endothelial cell elongation. The elongation required VEGF at a low concentration, which was insufficient to elicit the same effect by itself. The elongation also depended on Foxo1, a transcription factor indispensable for angiogenesis. Interestingly, the Foxo1 dependency of the elongation was overridden by inhibition of mTORC1, but not by PI3K-Akt, under stimulation by a high concentration of VEGF. Dual inhibition of mTORC1 and mTORC2 failed to induce cell elongation, revealing mTORC2 as a positive regulator of elongation. Our findings suggest that the PI3K-Akt-Foxo1 and mTORC1-mTORC2 pathways differentially regulate endothelial cell elongation, depending on the microenvironmental levels of VEGF., The Company of Biologists
Journal of Cell Science, 2016年03月15日, ［査読有り］ - Molecular Pathways Governing Development of Vascular Endothelial Cells from ES/iPS Cells
Keai Sinn Tan; Kiyomi Tamura; Mei I Lai; Abhimanyu Veerakumarasivam; Yoichi Nakanishi; Minetaro Ogawa; Daisuke Sugiyama, Assembly of complex vascular networks occurs in numerous biological systems through morphogenetic processes such as vasculogenesis, angiogenesis and vascular remodeling. Pluripotent stem cells such as embryonic stem (ES) and induced pluripotent stem (iPS) cells can differentiate into any cell type, including endothelial cells (ECs), and have been extensively used as in vitro models to analyze molecular mechanisms underlying EC generation and differentiation. The emergence of these promising new approaches suggests that ECs could be used in clinical therapy. Much evidence suggests that ES/iPS cell differentiation into ECs in vitro mimics the in vivo vascular morphogenic process. Through sequential steps of maturation, ECs derived from ES/iPS cells can be further differentiated into arterial, venous, capillary and lymphatic ECs, as well as smooth muscle cells. Here, we review EC development from ES/iPS cells with special attention to molecular pathways functioning in EC specification., Springer Science and Business Media LLC
Stem Cell Reviews and Reports, 2013年06月14日, ［査読有り］ - ABCA12 dysfunction causes a disorder in glucosylceramide accumulation during keratinocyte differentiation
Susumu Mitsutake; Chihiro Suzuki; Masashi Akiyama; Kiyomi Tsuji; Teruki Yanagi; Hiroshi Shimizu; Yasuyuki Igarashi, Harlequin ichthyosis (HI) is an autosomal recessive congenital ichthyoses, and patients of this disease frequently present with severe hyperkeratosis and scales over all of their epidermal surfaces. Recently, the gene encoding ABCA12 was identified as a causative gene for HI. Since dysfunction in ABCA12 causes a decrease in epidermal ceramide (Cer) content concomitantly with loss of the skin lipid barrier, ABCA12 is thought to regulate epidermal generation of Cer. However, so far no direct target of ABCA12 has been identified. Thus, we attempted to study the substrate of ABCA12 by generating an ABCA12-deficient keratinocyte cell line and then comparing its sphingolipid metabolism to that of a normal keratinocyte cell line., Elsevier BV
Journal of Dermatological Science, 2010年11月, ［査読有り］ - Leptin stimulates fibroblast growth factor 23 expression in bone and suppresses renal 1α,25-dihydroxyvitamin D3 synthesis in leptin-deficient ob/ob Mice
Kiyomi Tsuji; Toyonobu Maeda; Tetsuya Kawane; Ayako Matsunuma; Noboru Horiuchi, 筆頭著者, Leptin is the LEP (ob) gene product secreted by adipocytes. We previously reported that leptin decreases renal expression of the 25-hydroxyvitamin D3 1α-hydroxylase (CYP27B1) gene through the leptin receptor (ObRb) by indirectly acting on the proximal tubules. This study focused on bone-derived fibroblast growth factor 23 (FGF-23) as a mediator of the influence of leptin on renal 1α-hydroxylase mRNA expression in leptin-deficient ob/ob mice. Exposure to leptin (200 ng/mL) for 24 hours stimulated FGF-23 expression by primary cultured rat osteoblasts. Administration of leptin (4 mg/kg i.p. at 12-hour intervals for 2 days) to ob/ob mice markedly increased the serum FGF-23 concentration while significantly reducing the serum levels of calcium, phosphate, and 1α,25-dihydroxyvitamin D3 [1,25(OH)2D3]. Administration of FGF-23 (5 µg i.p. at 12-hour intervals for 2 days) to ob/ob mice suppressed renal 1α-hydroxylase mRNA expression. The main site of FGF-23 mRNA expression was the bone, and leptin markedly increased the FGF-23 mRNA level in ob/ob mice. In addition, leptin significantly reduced 1α-hydroxylase and sodium-phosphate cotransporters (NaPi-IIa and NaPi-IIc) mRNA levels but did not affect Klotho mRNA expression in the kidneys of ob/ob mice. Furthermore, the serum FGF-23 level and renal expression of 1α-hydroxylase mRNA were not influenced by administration of leptin to leptin receptor–deficient (db/db) mice. These results indicate that leptin directly stimulates FGF-23 synthesis by bone cells in ob/ob mice, suggesting that inhibition of renal 1,25(OH)2D3 synthesis in these mice is at least partly due to elevated bone production of FGF-23. ＊Faculty of 1000 (F1000) 推薦, Oxford University Press (OUP)
Journal of Bone and Mineral Research, 2010年07月30日, ［査読有り］ - Hematopoiesis from pluripotent stem cell lines
Hiroshi Sakamoto; Kiyomi Tsuji-Tamura; Minetaro Ogawa, Embryonic stem cells (ESCs) can differentiate into various types of hematopoietic cells (HPCs) when placed in an appropriate environment. Various methods for the differentiation of ESCs into specific HPC lineages have been developed using mouse ESCs. These ESC-differentiation methods have been utilized also as an in vitro model to investigate hematopoiesis in embryos and they provided critical perceptions into it. These methods have been adapted for use with human ESCs, which have the possibility of being employed in regenerative medicine; further improvement of these methods may lead to the efficient production of HPCs for use in transfusions. The generation of transplantable hematopoietic stem cells is a medical goal that is still difficult to achieve. Recently, induced pluripotent stem (iPS) cells have been established from differentiated cells. Thereby, iPS cells have expanded further possibilities of the use of pluripotent stem cell lines in clinical application. Indeed, iPS cells have been established from cells with disease genes and those which have undergone reprogramming and targeting have generated phenotypically normal HPCs. Here, we mainly summarize the recent progress in research on hematopoiesis conducted with ESCs and iPS cells., Springer Science and Business Media LLC
International Journal of Hematology, 2010年02月20日, ［査読有り］ - Foxo1 is essential for in vitro vascular formation from embryonic stem cells.
Seung-Hwan Park; Hiroshi Sakamoto; Kiyomi Tsuji-Tamura; Tatsuo Furuyama; Minetaro Ogawa, The forkhead transcription factors regulate the correct organization of vascular system. One of them, Foxo1 is an important physiological regulator of endothelial cell morphology in response to VEGF, while underlying mechanisms are largely unknown. In order to elucidate the cellular function of Foxo1, we used a three-dimensional culture system for the differentiation of Flk1-expressing mesodermal precursor cells derived from ES cells to cord forming endothelial cells and associating vascular smooth muscle cells. While Foxo1(+/+) endothelial cells organized into long vessel-like structures associated with smooth muscle cells, Foxo1(-/-) endothelial cells could form only short sprouts. Foxo1(-/-) endothelial cells have punctate accumulation of filamentous actin, thick circumferential bundles of microtubules with small spikes at the tip of cells, and no interaction with smooth muscle cells. Our results suggest the involvement of Foxo1 in cytoskeletal remodeling of endothelial cells and recruitment of smooth muscle cells during vascular development.
Biochemical and biophysical research communications, 2009年12月18日, ［査読有り］ - Ceramide biosynthesis in keratinocyte and its role in skin function
Yukiko Mizutani; Susumu Mitsutake; Kiyomi Tsuji; Akio Kihara; Yasuyuki Igarashi, The enucleate layer of the epidermis, i.e. the stratum corneum, is responsible for certain critical protective functions, such as epidermal permeability barrier function. Within the epidermal membrane lamella component, ceramides are the dominant lipid class by weight (over 50%) and exhibit the greatest molecular heterogeneity in terms of sphingoid base and fatty acid composition. It is now evermore important to understand how ceramide production and functions are controlled in the epidermis, since decreased epidermal ceramide content has been linked to water loss and barrier dysfunction. During the past several years, critical enzymes in ceramide biosynthesis have been identified, including ceramide synthases (CerS) and ceramide hydroxylase/desaturase. In this review, we describe the molecular heterogeneity of ceramides synthesized in the epidermis and their possible roles in epidermal permeability barrier functions. We also describe recent studies that identified the family of CerS (CerS1-CerS6) in mammals. We further focus on the roles of specific isoforms of these enzymes in synthesizing the epidermal ceramides, especially in relation to chain-length specificity. In addition, we provide experimental information, including our recent findings, as to how applying ceramide or ceramide-containing substances to skin, orally or directly, can benefit skin health., Elsevier BV
Biochimie, 2009年06月, ［査読有り］ - Evaluation of synthetic sphingolipid analogs as ligands for peroxisome proliferator-activated receptors
Kiyomi Tsuji; Shigeru Satoh; Susumu Mitsutake; Itsuo Murakami; Jeong-Ju Park; Qian Li; Young-Tae Chang; Sung-Kee Chung; Yasuyuki Igarashi, 筆頭著者, In this Letter, we assessed newly synthesized sphingolipid analogs as ligands for peroxisome proliferator-activated receptor (PPAR)alpha, PPARbeta or PPARgamma, using a dual-luciferase reporter system. We tested 640 sphingolipid analogs for ligand activity. As a result, seven types: A9, B9, C9, C50, F66, G66 and H66, were found to show agonistic activities for PPARs., Elsevier BV
Bioorganic & Medicinal Chemistry Letters, 2009年03月15日, ［査読有り］ - Role of ceramide kinase in peroxisome proliferator‐activated receptor beta‐induced cell survival of mouse keratinocytes
Kiyomi Tsuji; Susumu Mitsutake; Urara Yokose; Masako Sugiura; Takafumi Kohama; Yasuyuki Igarashi, 筆頭著者, Ceramide (Cer) is known to be a lipid mediator in apoptosis and to have an important role in cell fate, via control of intracellular Cer levels. Recently, ceramide kinase (CerK) was identified as an enzyme that converts Cer to ceramide 1‐phosphate (C1P). We examined potential functions of CerK in the regulation of keratinocyte survival, and the possible involvement of peroxisome proliferator‐activated receptor beta (PPARβ). PPARβ is known to be a nuclear receptor acting as a ligand‐inducible transcription factor and has been implicated in the control of keratinocyte survival. In the mouse keratinocyte cell line SP1, serum starvation induced cell death and the accumulation of intracellular Cer, an apoptotic event. However, apoptosis was inhibited by activation of PPARβ. Interestingly, activation of PPARβ enhanced the mRNA expression of CerK and CerK activity. Furthermore, the cell survival effect of PPARβ was greatly diminished in keratinocytes isolated from CerK‐null mice. Chromatin immunoprecipitation revealed that, in vivo, PPARβ binds to the CerK gene via a sequence located in the first intron. Electrophoretic mobility‐shift assays confirmed that PPARβ associates with this sequence in vitro. These findings indicated that CerK gene expression was directly regulated by PPARβ. In conclusion, our results demonstrate that PPARβ‐mediated upregulation of CerK gene expression is necessary for keratinocyte survival against serum starvation‐induced apoptosis., Wiley
The FEBS Journal, 2008年07月11日, ［査読有り］ - タモギタケエタノール抽出物のアトピー性皮膚炎モデルマウスを用いた保湿作用およびアトピー様症状に対する作用
冨山 隆広; 海方 忍; 石田 真己; 西川 英俊; 山崎 則之; 辻 潔美; 光武 進; 五十嵐 靖之, アトピー性皮膚炎患者のほとんどは，乾燥肌，バリア機能の低下および皮膚炎症状がみられる。HR-1ヘアレスマウスは，皮膚にダメージを与える特殊な誘導食（HR-AD）によって，アトピー性皮膚炎様所見を示すことが知られている。本研究では，このモデルを用いて，グルコシルセラミドを高濃度含有するタモギタケエタノール抽出物（以下，タモギタケエキス，と記載する）の混餌投与がアトピー性皮膚炎様所見にどのような影響を与えるかを検討した。その結果，対照群（HR-AD投与群）では，皮膚水分蒸散量（TEWL）の経時的増加，角化亢進および真皮への細胞浸潤が認められるなど，典型的なアトピー性皮膚炎様所見を示した。それに対してタモギタケエキス投与群では，アトピー性皮膚炎様所見についていずれも改善する効果を示した（タモギタケエキスの投与量はセラミドとして0.1%および0.01%）。タモギタケエキスの混餌投与は，アトピー性皮膚炎モデルマウスを用いた実験系において，皮膚のバリアー機能を改善し，対照群で認められた皮膚炎症状の発症を抑制する作用を示したと予想される。, 日本栄養・食糧学会
日本栄養・食糧学会誌, 2008年, ［査読有り］ - Dietary glucosylceramide improves skin barrier function in hairless mice
Kiyomi Tsuji; Susumu Mitsutake; Junko Ishikawa; Yutaka Takagi; Masashi Akiyama; Hiroshi Shimizu; Takahiro Tomiyama; Yasuyuki Igarashi, 筆頭著者, Background: Sphingolipids are known to play an important role in both water retention and epidermal permeability barrier function in mammalian stratum corneum. However, little is known about the effects on epidermal function of orally administered sphingolipids.
Objective: We examined the effect of dietary glucosylceramide (GluCer) on the maintenance and recovery of epidermal barrier function.
Methods: Hairless mice were fed a particular diet (HR-AD) for 4 weeks to induce chronic skin perturbation. Subsequently, a normal diet supplemented with GluCer (from rice bran and germ) was provided for the next 4 weeks. Transepidermal water loss (TEWL) and stratum corneum flexibility were measured throughout this recovery phase. Additional hairless mice were fed a diet with or without a maize-extracted GluCer supplement for 5 weeks, then their skin was acutely perturbed with repeated tape-stripping, and the TEWL was measured.
Results: Although skin functions were generally lower following chronic perturbation, in GluCer-fed mice the TEWL was significantly reduced at 2 weeks and the stratum corneum flexibility was increased at 3 weeks compared to controls. Following acute barrier perturbation by tape-stripping, mice an HR-AD fed a GluCer diet exhibited enhanced recovery compared with the control diet group.
Conclusion: These results demonstrate that in hairless mice skin barrier functions impaired by chronic or acute perturbations were improved by dietary GluCer. The oral administration of GluCer may be useful for the preservation and recovery of epidermal barrier functions an HR-AD., Elsevier BV
Journal of Dermatological Science, 2006年11月, ［査読有り］ - Apoptosis Occurs via the Ceramide Recycling Pathway in Human HaCaT Keratinocytes
Saeko Takeda; Susumu Mitsutake; Kiyomi Tsuji; Yasuyuki Igarashi, Keratinocytes contain abundant ceramides compared to other cells. However, studies on these cells have mainly focused on the barrier function of ceramide, while their other roles, such as those in apoptosis or cell cycle arrest, have not been well addressed. In this study, we investigated the apoptosis-inducing effect of exogenously added cell-permeable ceramides in HaCaT keratinocytes. We found that N-hexanoyl sphingosine (C6-ceramide) induced apoptosis efficiently through the accumulation of long chain ceramides. On the other hand, N-acetyl sphingosine (C2-ceramide) induced neither apoptosis nor accumulation of long chain ceramides. We also found that exogenously added C6-ceramide was hydrolyzed to sphingosine and then reacylated in long chain ceramides (ceramide recycling pathway), but that C2-ceramide was not hydrolyzed and thus not recycled. We propose that this is the basis for the chain length-specific heterogeneity observed in ceramide-induced apoptosis in these cells. These results also imply that keratinocytes utilize exogenous sphingolipids or ceramides to coordinate their own ceramide compositions., Oxford University Press (OUP)
The Journal of Biochemistry, 2006年02月01日, ［査読有り］ - Regulation of mRNA Expression of Matrix Extracellular Phosphoglycoprotein (MEPE)/ Osteoblast/Osteocyte Factor 45 (OF45) by Fibroblast Growth Factor 2 in Cultures of Rat Bone Marrow–Derived Osteoblastic Cells
Gui Xia Zhang; Morimichi Mizuno; Kiyomi Tsuji; Masato Tamura, Matrix extracellular phosphoglycoprotein (MEPE)/ osteoblast/osteocyte factor 45 (OF45) is a recently isolated RGD-containing matrix protein that acts as the tumor-derived phosphaturic factor in oncogenic hypophosphatemic osteomalacia. It is also highly expressed by osteoblasts and osteocytes. We examined the regulation of MEPE/OF45 mRNA expression in osteoblastic cells derived from high-density cultures of primary rat bone marrow stromal cells incubated with dexamethasone, beta-glycerophosphate, and ascorbic acid. The level of MEPE/OF45 mRNA in these cells was down-regulated by the addition of fibroblast growth factor 2 (FGF2) for 48 h. These effects were observed in a dose-dependent manner between 2 and 10 ng/mL. FGF2 also reduced the expression of osteocalcin mRNA in these cells. In contrast, bone sialoprotein mRNA expression was increased by FGF2, while alpha1(I) procollagen mRNA expression was not altered. Additionally, neither Runx2 and osterix mRNA expression nor cell proliferation were affected by the addition of FGF2 in these high-density cultures, indicating that regulation by FGF2 may not be dependent on these transcription factors or on the proliferation of cells. Experiments using actinomycin D indicated that FGF2 decreased the stability of the MEPE/OF45 mRNA. Moreover, inhibition of a specific mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase kinase (MEK) by PD98059 blocked FGF2-regulated MEPE/OF45 expressions, indicating that this regulation requires the MAPK pathway. These results suggest that MEPE/OF45 gene is one of the targets of FGF2 and may play an important role during bone formation and calcification., Springer Science and Business Media LLC
Endocrine, 2004年06月, ［査読有り］ - Periodontal ligament cells under intermittent tensile stress regulate mRNA expression of osteoprotegerin and tissue inhibitor of matrix metalloprotease-1 and -2
Kiyomi Tsuji; Keiji Uno; Gui Xia Zhang; Masato Tamura, 筆頭著者, We studied the mRNA expression of osteoprotegerin (OPG), receptor activator of NF-kappa B ligand (RANKL), tissue inhibitor of matrix metalloprotease (TIMP)-1 and -2, and matrix metalloprotease (MMP)-1 and -2 by human periodontal ligament (PDL) cells under intermittent tensile stress using a Flexercell Strain Unit. Analysis by reverse transcriptase-polymerase chain reaction showed that mechanical force upregulated OPG mRNA. We also demonstrated that the protein concentration of OPG in conditioned medium increased upon loading with tensile stress, as determined by enzyme-linked immunosorbent assay. TIMP-1 and -2 mRNA levels also increased, whereas levels of RANKL, MMP-1, and MMP-2 mRNA were barely affected. We further examined the effect of loading with tensile stress and addition of Salmonella abortus equi lipopolysaccharide (LPS) on the mRNA expression of PDL cells. The amount of OPG mRNA induced by mechanical strain was found to decrease with the addition of LPS to cultures. The induction of OPG mRNA expression by stretching was inhibited in the presence of indomethacin or genistein, whereas TIMP-1 mRNA expression induced by stretching was inhibited by the addition of cycloheximide, suggesting that tensile stress regulates cyclooxygenase activities, tyrosine phosphorylation, and de novo protein synthesis in PDL cells through the induction of OPG and TIMP-1 mRNA expression. These results provide evidence that the mechanical stimulus of stretching is responsible for the observed regulation of bone resorption and tissue degradation in PDL tissue., Springer Science and Business Media LLC
Journal of Bone and Mineral Metabolism, 2004年03月, ［査読有り］
MISC
- 転写因子FOXO1によるリン酸化ミオシン軽鎖2(MLC2)を介した血管新生の促進機構
田村(辻)潔美
Journal of Oral Biosciences Supplement (Web), 2024年 - RNA-sequencingを用いた骨細胞におけるメカニカルストレス応答機構の解析
藤田尚正; 藤田尚正; 田村(辻)潔美; 田村正人; 佐藤真理
Journal of Oral Biosciences Supplement (Web), 2021年 - 血管発生におけるグリシン二相性効果に関与するシグナル伝達経路
田村(辻)潔美; 佐藤真理; 田村正人
Journal of Oral Biosciences Supplement (Web), 2021年 - 血管内皮細胞におけるmTORC1/mTORC2阻害剤の効果
田村 潔美; 田村 正人; 小川 峰太郎
Journal of Oral Biosciences Supplement, 2018年09月 - 血管内皮細胞の伸張機能に着目した、血管形成の新たな指標の探索
田村 潔美; 田村 正人; 小川 峰太郎
Journal of Oral Biosciences Supplement, 2017年09月 - PI3K-AktとmTORC1シグナルは血管内皮細胞の伸長機能を制御する
田村 潔美; 田村 正人; 小川 峰太郎
Journal of Oral Biosciences Supplement, 2016年09月 - Neuropeptide Y Y1受容体の阻害によるMC3T3-E1細胞における骨芽細胞分化の誘導
箭原元基; 田村(辻)潔美; 田村正人
Journal of Oral Biosciences Supplement (Web), 2016年 - PI3K-AktとmTORC1シグナルは血管内皮細胞の伸長機能を制御する
田村(辻)潔美; 田村正人
Journal of Oral Biosciences Supplement (Web), 2016年 - 胚性幹細胞からの二機能性造血内皮細胞の同定
AHMED Tanzir; HIROTA Saeka; TSUJI-TAMURA Kiyomi; OGAWA Minetaro
日本分子生物学会年会プログラム・要旨集(Web), 2014年 - 休眠造血幹細胞はc-Myb蛋白質を低レベルに抑制する
SAKAMOTO Hiroshi; TAKEDA Naoki; TSUJI-TAMURA Kiyomi; HIROTA Saeka; HASHIGUCHI Atsushi; AHMED Tanzir; OGAWA Minetaro
臨床血液, 2013年 - 造血幹細胞におけるc-Mybの発現及び機能
SAKAMOTO Hiroshi; TAKEDA Naoki; GARCIA Paloma; TSUJI-TAMURA Kiyomi; HIROTA Saeka; FRAMPTON Jon; OGAWA Minetaro
臨床血液, 2012年 - Foxo1は胚性幹細胞からのin vitro血管形成に必須である
PARK Seung-Hwan; SAKAMOTO Hiroshi; TSUJI-TAMURA Kiyomi; FURUYAMA Tatsuo; OGAWA Minetaro
Program and Abstract Book. Annual Meeting for the Japanese Society of Developmental Biologists, 2010年 - マウス表皮細胞のcell survivalにおける,核内受容体PPAR βを介したセラミドキナーゼ(CERK)遺伝子発現の調節機能
辻潔美; 堀内登
Journal of Oral Biosciences, 2008年 - マウスケラチン細胞株(SP1細胞)における核受容体ペルオキソーム増殖活性化受容体ベータ(PPARβ)セラミドキナーゼ(CERK)遺伝子発現
TSUJI Kiyomi; MITSUTAKE Susumu; IGARASHI Yasuyuki
生化学, 2006年
書籍等出版物
- Embryonic Stem Cells: The Hormonal Regulation of Pluripotency and Embryogenesis
Kiyomi Tsuji-Tamura; Hiroshi Sakamoto; Minetaro Ogawa, 分担執筆
IntechOpen, 2011年04月26日, ［査読有り］
9789533071961
講演・口頭発表等
- FOXO1-mediated phosphorylation of myosin light chain 2 promotes endothelial cell elongation and angiogenesis
Kiyomi Tsuji-Tamura; Minetaro Ogawa
第33回日本血管生物医学会学術集会 併催: The 6th Asia-Australia Vascular Biology Meeting 2025, 2025年11月01日
20251101, 20251102 - MYL9による内皮細胞の形態制御と血管新生における機能的役割
田村-辻 潔美; 李 智媛
第67回歯科基礎医学会学術大会, 2025年09月07日 - FOXO1 transcription factor promotes angiogenesis via myosin light chain 2 (MLC2) phosphorylation
Kiyomi Tsuji-Tamura
HIGO Cutting-Edge Seminar, 2025年01月22日, Institute of Molecular Embryology and Genetics, Kumamoto University, ［招待有り］ - 転写因子FOXO1によるリン酸化ミオシン軽鎖2(MLC2)を介した血管新生の促進機構
田村-辻 潔美
第66回歯科基礎医学会学術大会, 2024年11月03日 - 転写因子FOXO1のミオシン軽鎖2のリン酸化を介した血管内皮細胞の伸長と血管新生の促進
田村-辻潔美; 小川峰太郎
第45回日本炎症・再生医学会, 2024年07月17日 - 平滑筋マーカーであるTAGLNの血管内皮細胞における新たな役割
田村-辻 潔美
第46回日本分子生物学会年会 シンポジウム: ⼼⾎管系を⽀える細胞遷移ダイナミクス, 2023年12月07日, ［招待有り］
20231206, 20231208 - bFGFは血管平滑筋細胞の静止状態を解除する
田村-辻 潔美
第9回北大部局横断シンポジウム, 2023年10月11日 - ミオシン軽鎖のリン酸化を介した血管新生の薬剤によるコ ントロール
田村-辻 潔美; 田村 正人
第65回歯科基礎医学会学術大会, 2023年09月17日 - 血管平滑筋細胞の静止状態を解除する因子の探索：動脈硬化の観点から
田村-辻潔美; 田村 正人
第44回日本炎症・再生医学会, 2023年07月12日 - 平滑筋マーカーであるSM22(TAGLN)の血管内皮細胞における新たな役割
田村-辻 潔美
第8回 北海道大学部局横断シンポジウム, 2022年10月28日 - bFGFは静止期の血管平滑筋細胞を特異的に刺激し増殖と脱分化を誘導する
田村-辻 潔美; 田村 正人
第64回歯科基礎医学会学術大会, 2022年09月19日 - 平滑筋マーカーとして知られるＳＭ２２は血管内皮細胞の伸長機能を抑制し血管新生を負に 制御する
田村-辻 潔美; 古賀 沙緒里; 小川 峰太郎
第43回日本炎症・再生医学会, 2022年07月06日 - ゼブラフィッシュ血管発生におけるグリシンの用量依存的二相性効果
田村-辻 潔美
第7 回ゼブラフィッシュ・メダカ創薬研究会, 2021年12月03日, ［招待有り］ - RNA-sequencing を用いた骨細胞におけるメカニカルストレス応答機構の解析
藤田 尚正; 田村-辻 潔美; 田村 正人; 佐藤 真理
第63回歯科基礎医学会学術大会, 2021年10月11日 - 血管発生におけるグリシン二相性効果に関与するシグナル伝達経路
田村- 潔美; 佐藤 真理; 田村 正人
第63回歯科基礎医学会学術大会, 2021年10月10日 - ゼブラフィッシュの血管発生におけるグリシンの二相性効果
田村-辻 潔美
第7回北海道大学部局横断シンポジウム, 2021年10月01日 - 血管発生におけるグリシンの用量依存的二相性効果
田村-辻 潔美; 佐藤 真理; 田村 正人
第62回歯科基礎医学会学術大会, 2020年09月12日 - Elongation of vascular endothelial cells is accompanied by activation of the SM22 gene, a canonical marker of smooth muscle cells
Kiyomi Tsuji-Tamura; Minetaro Ogawa
Key Forum: The 3rd International Symposium on Stem Cell Traits and Developmental Systems, 2018年11月11日 - 血管内皮細胞におけるmTORC1/mTORC2阻害剤の効果
田村-辻 潔美; 田村 正人
第60回歯科基礎医学会学術大会, 2018年09月06日 - 血管内皮細胞の細胞骨格と細胞伸張に対するmTORC1/mTORC2阻害剤の抑制効果
田村-辻潔美; 田村 正人; 小川峰太郎
第39回日本炎症・再生医学会, 2018年07月11日 - VEGF濃度依存性の二つの経路による血管伸張の制御機構
田村-辻 潔美; 田村 正人
第3回北海道大学部局間横断シンポジウム, 2018年01月26日 - The induction of vascular endothelial cell elongation without an overdose of vascular endothelial growth factor (VEGF)
Kiyomi Tsuji-Tamura
the International Association for Dental Research (IADR), 2017年11月18日 - 血管内皮細胞の伸張機能に着目した，血管形成の新たな指標の探索
田村-辻 潔美; 田村 正人
第59回歯科基礎医学会学術大会, 2017年09月17日 - 血管内皮細胞の伸張に伴うSM22(TAGLN)の発現－血管形成の指標としての可能性
田村-辻 潔美
第38回日本炎症・再生医学会, 2017年07月19日 - 血管伸張は、VEGF濃度に依存して異なる二つの経路で調節される
田村-辻潔美; 田村正人
第５４回日本生化学会北海道支部例会 日本生化学会北海道支部・日本生物物理学会北海道支部合同シンポジウム, 2017年07月07日 - PI3K−Akt と mTORC1 シグナルは血管内皮細胞の伸長機能を制御する
田村-辻 潔美; 田村 正人
第58回歯科基礎医学会学術大会, 2016年08月26日 - Neuropeptide Y Y1 受容体の阻害による MC3T3-E1 細胞における骨芽細胞分化の誘導
箭原 元基; 田村-辻 潔美; 田村 正人
第58回歯科基礎医学会学術大会, 2016年08月25日 - 血管伸長を誘導する2つの経路：PI3K/Akt/Foxo1とmTORC1
田村-辻 潔美; 小川 峰太郎
第36回日本炎症・再生医学会, 2015年07月21日 - Identification of bipotential hemogenic endothelial cells from embryonic stem cell culture
Tanzir Ahmed; Saeka Hirota; Kiyomi Tamura; Minetaro Ogawa
KEY Forum: From Stem Cells to Organs, 2014年09月04日 - The role of Foxo1 transcription factor in vascular development
Kiyomi Tsuji-Tamura; Minetaro Ogawa
KEY Forum: From Stem Cells to Organs, 2014年09月04日 - Foxo1 transcription factor regulates endothelial cell morphology by controlling phosphorylation of myosin light chain
Kiyomi Tsuji-Tamura:Hiroshi Sakamoto:Minetaro Ogawa
The 18th International Vascular Biology Meeting (IVBM), 2014年04月14日 - Foxo1 transcription factor regulates endothelial cell morphology by controlling phosphorylation of myosin light chain
Kiyomi Tsuji-Tamura; Hiroshi Sakamoto; Minetaro Ogawa
第2回IRG (Inflammation and ReGeneration) Meeting, 2014年01月17日 - 転写因子Ｆｏｘｏ１による血管内皮細胞の形態制御メカニズムの解析
田村-辻 潔美; 坂本 比呂志; 小川 峰太郎
第34回日本炎症・再生医学会, 2013年07月02日 - 管内皮細胞の形態制御に関与する転写因子Ｆｏｘｏ１の標的因子の探索
田村-辻 潔美; 坂本 比呂志; 小川 峰太郎
第33回日本炎症・再生医学会, 2012年07月05日 - Forkhead transcriptional factor 1 (Foxo1) regulates vascular endothelial cell morphology
田村-辻 潔美
５拠点シンポジウム, 2012年02月04日 - 転写因子Ｆｏｘｏ１は血管形成制御に関与している
田村-辻 潔美; 坂本 比呂志; 小川 峰太郎
第2回 Molecular Cardiovascular Conference Ⅱ, 2011年09月03日 - 血管特異的エンハンサー配列を用いた血管前駆細胞系譜の解析
田村-辻 潔美; 坂本 比呂志; 小川 峰太郎
第32回日本炎症・再生医学会, 2011年06月02日 - The role of Foxo1 transcription factor in vascular development
Tsuji-Tamura Kiyomi; Hiroshi Sakamoto; Seunghwan Park; Minetaro Ogawa
第8回心血管幹細胞研究会, 2011年01月14日 - Vascular endothelial cell-lineage analysis by an endothelial-specific enhancer element
Kiyomi Tamura
2010 Global COE-IMEG Joint Summer Retreat Seminar in Aso, 2010年09月09日 - 転写因子Ｆｏｘｏ１は血管内皮細胞における細胞形態制御に関与する
田村-辻 潔美; 坂本 比呂志; 小川 峰太郎
第31回日本炎症・再生医学会, 2010年08月05日
所属学協会
共同研究・競争的資金等の研究課題
社会貢献活動
学術貢献活動
- 学術論文査読
査読
2023年: Food and Chemical Toxicology, Life sciences. 2024年: Life sciences, Next research, Life sciences, Heliyon, Biochemical and biophysical research communications. 2025年: Computers in biology and medicine, Tohoku Journal of Experimental Medicine, Experimental Cell Research, Life sciences, 2026年: Tohoku Journal of Experimental Medicine, Cell Biology and Toxicology, 2023年 - 現在 - 日本生化学会北海道支部・日本生物物理学会北海道支部合同シンポジウム「生命現象の分子レベルでの解明」
企画立案・運営等
日本生化学会北海道支部, 2016年07月08日
