作者: Kenji Sobue , Ken’ichiro Hayashi , Wataru Nishida
DOI: 10.1007/978-1-4615-5543-8_14
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摘要: Phenotypic modulation of smooth muscle cells (SMCs) plays an integral role in atherosclerosis, hypertension and leiomyogenic tumorigenicity. The morphological, functional, biochemical characteristics SMCs different phenotypes such as differentiated dedifferentiated states have been well studied. Recent researches focused on the expressional regulation SMC-specific marker genes association with phenotypic SMCs. are regulated at levels transcription splicing. caldesmon, myosin heavy chain, α-smooth actin, calponin, SM22, α- β-tropomyosins, a1 integrin transcriptionally regulated; these except for actin gene is upregulated SMCs, but downregulated expression pattern opposite vascular visceral In almost all promoter regions genes, CArG box serum response factor (SRF) involved positive cis-element trans-acting factor, respectively. Isoform changes α-tropomyosin, vinculin/metavinculin, chain by alternative splicing a SMC phenotype-dependent manner. Among them, isoform interconversions caldesmon α-tropomyosin completely coordinated phenotype purpose this paper to summarize current knowledge