2014 Fiscal Year Final Research Report
Molecular mechanisms of the association between .t2DM and Tskotudo
Project/Area Number |
24390194
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Partial Multi-year Fund |
Section | 一般 |
Research Field |
Circulatory organs internal medicine
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Research Institution | Gunma University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
ISO Tatsuya 群馬大学, 大学院医学系研究科, 准教授 (10400756)
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Project Period (FY) |
2012-04-01 – 2015-03-31
|
Keywords | 血管石灰化 / 血管平滑筋細胞 / リン / Klotho / オステオプロテジェリン |
Outline of Final Research Achievements |
Both clinical and basic research demonstrated conflicting evidence regarding the pathophysiological role of Fibroblast growth factor 23 (FGF23) concentration in vascular calcification. We determine the effects of FGF23 on the osteoblastic gene expression in vascular smooth muscle cells (VSMC). HASMC transduced with adenovirus expressing human FGF23 (Ad-FGF23) exhibited a significant decrease in the expression of the osteoblast-marker genes. Of note, Ad-FGF23 increased mRNA and protein levels for osteoprotegerin (OPG), and human OPG promoter was activated by FGF23. FGF23 up-regulated OPG expression, whereas depletion of Klotho by siRNA attenuated FGF23-induced OPG expression. These results indicate that FGF23 suppresses osteoblastic gene expression and induces OPG expression in HASMC, and support the hypothesis that FGF23 counteracts the osteogenic conversion of vascular SMC as a component of compensatory mechanisms to mitigate the vascular calcification.
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Free Research Field |
循環器内科学
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