Regulation of vascular smooth muscle cell differentiation by fatty acid composition
Project/Area Number |
16H05294
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Cardiovascular medicine
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Research Institution | Gunma University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
磯 達也 群馬大学, 大学院医学系研究科, 研究員 (10400756)
|
Project Period (FY) |
2016-04-01 – 2019-03-31
|
Project Status |
Completed (Fiscal Year 2018)
|
Budget Amount *help |
¥17,680,000 (Direct Cost: ¥13,600,000、Indirect Cost: ¥4,080,000)
Fiscal Year 2018: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2017: ¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2016: ¥10,140,000 (Direct Cost: ¥7,800,000、Indirect Cost: ¥2,340,000)
|
Keywords | 動脈硬化 / 血管平滑筋 / エネルギー代謝 / 脂肪酸 / 血管平滑筋細胞 / 形質変換 / 転写因子 / 糖尿病 / KLF4 / AMPK |
Outline of Final Research Achievements |
We investigated the role of elongation of long-chain fatty acid (LCFA) member 6 (Elovl6), a rate-limiting enzyme catalyzing the elongation of saturated and monounsaturated LCFA, in the regulation of phenotypic switching of VSMC.We demonstrate for the first time that dysregulation of Elovl6-driven LCFA metabolism induces phenotypic switching of VSMC via ROS production and AMPK/KLF4 signaling that leads to growth arrest and downregulation of VSMC marker expression. The modulation of Elovl6-mediated cellular processes may provide an intriguing approach for tackling atherosclerosis and post-angioplasty restenosis.
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Academic Significance and Societal Importance of the Research Achievements |
本研究の成果は、血管平滑筋細胞に留まらず、さまざまな細胞における脂肪酸代謝の変化が細胞の増殖や分化調節にどのような役割を持つかに関しての研究と繋がり、再生医学やがん細胞の生物学にも波及しうる成果を提供しうると考えている。
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Report
(4 results)
Research Products
(15 results)
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[Journal Article] Circulating FABP4 is eliminated by the kidney via glomerular filtration followed by megalin-mediated reabsorption2018
Author(s)
Shrestha S, Sunaga H, Hanaoka H, Yamaguchi A, Kuwahara S, Umbarawan Y, Nakajima K, Machida T, Murakami M, Saito A, Tsushima Y, Kurabayashi M, Iso T
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Journal Title
Sci Rep
Volume: 8(1)
Issue: 1
Pages: 16451-16451
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] CD36 is indispensable for nutrient homeostasis and endurance exercise capacity during prolonged fasting2018
Author(s)
Iso T, Haruyama H, Sunaga H, Matsui H, Matsui M, Tanaka R, Umbarawan Y, Syamsunarno MRAA, Putri M, Yamaguchi A, Hanaoka H, Negishi K, Yokoyama T, Kurabayashi M
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Journal Title
Physiol Rep
Volume: 6(19)
Issue: 19
Pages: e13884-e13884
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] Myocardial fatty acid uptake through CD36 is indispensable for sufficient bioenergetic metabolism to prevent progression of pressure overload-induced heart failure2018
Author(s)
Umbarawan Y, Syamsunarno MRAA, Koitabashi N, Obinata H, Yamaguchi A, Hanaoka H, Hishiki T, Hayakawa N, Sano M, Sunaga H, Matsui H, Tsushima Y, Suematsu M, Kurabayashi M, Iso T
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Journal Title
Sci Rep
Volume: 8(1)
Issue: 1
Pages: 12035-12035
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] Glucose is preferentially utilized for biomass synthesis in pressure-overloaded hearts: Evidence from fatty acid binding protein-4 and -5 knockout mice.2018
Author(s)
Umbarawan Y, Syamsunarno MRAA, Koitabashi N, Yamaguchi A, Hanaoka H, Hishiki T, Nagahata-Naito Y, Obinata H, Sano M, Sunaga H, Matsui H, Tsushima Y, Suematsu M, Kurabayashi M, Iso T
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Journal Title
Cardiovasc Res.
Volume: -
Issue: 8
Pages: 1132-1144
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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[Journal Article] Robust suppression of cardiac energy catabolism with marked accumulation of energy substrates during lipopolysaccharide-induced cardiac dysfunction in mice.2017
Author(s)
Umbarawan Y, Syamsunarno MR, Obinata H, Yamaguchi A, Sunaga H, Matsui H, Hishiki T, Matsuura T, Koitabashi N, Obokata M, Hanaoka H, Haque A, Kunimoto F, Tsushima Y, Suematsu M, Kurabayashi M, Iso T
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Journal Title
Metabolism, clinical and experimental.
Volume: -
Pages: 47-57
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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