A study on the mechanism of dedifferentiation and hypertrophy of vascular myocytes in atherosclerotic lesions

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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