2002 Fiscal Year Final Research Report Summary
A study on the mechanism of dedifferentiation and hypertrophy of vascular myocytes in atherosclerotic lesions
| Project/Area Number |
13670695
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
SUZUKI Etsu The University of Tokyo, Faculty of Medicine, Research Associate, 医学部附属病院, 助手 (40313134)
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| Co-Investigator(Kenkyū-buntansha) |
NAGATA Daisuke The University of Tokyo, Faculty of Medicine, Medical Staff, 医学部附属病院, 医員
KAKOKI Masao The University of Tokyo, Faculty of Medicine, Medical Staff, 医学部附属病院, 医員
HIRATA Yasunobu The University of Tokyo, Faculty of Medicine, Lecturer, 医学部附属病院, 講師 (70167609)
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| Project Period (FY) |
2001 – 2002
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| Keywords | atherosclerosis / vascular myocytes / transcription factors |
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| Research Abstract |
We examined the roles of the transcription factors myocyte enhancer factor 2 (MEF2)- and nuclear factors of activated T cells (NFAT) in dedifferentiation and hypertrophy of vascular myocytes. Angiotensin II (ATII) induced the promoter activity of the nonmuscle-type myosin heavy chain B (NMMHCB) gene, which we used as a marker of the dedifferentiated state of VSMCs, and this increase was inhibited by calcineurin inhibitors, but not by the dominant negative mutants of MEF2A. Overexpression of a constitutively active calcineurin mutant stimulated the promoter activity of the NMMHCB gene. ATII increased protein synthesis and this increase was inhibited by infection with an adenovirus construct expressing the dominant nagative mutant of MEF2A, but not by calcineurin inhibitors. These results suggest that the MEF2- and calcineurin/NFAT-dependent pathways have distinct roles in vascular myocytes
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