Molecular mechanism of phenotypic modulation of smooth muscle cells

被引:37
作者
Sobue, K [1 ]
Hayashi, K [1 ]
Nishida, Q [1 ]
机构
[1] Osaka Univ, Sch Med, Biomed Res Ctr, Dept Neurochem & Neuropharmcol, Suita, Osaka 565, Japan
关键词
smooth muscle; phenotypic modulation; caldesmon; gene expression; splicing; contractile protein; alpha-smooth muscle actin; SM22; myosin heavy chain; alpha; 1; integrin; atherosclerosis;
D O I
10.1159/000053119
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Phenotypic modulation of smooth muscle cells is closely associated with vasculogenesis, enterogenesis and some diseases such as atherosclerosis, hypertension and leiomyogenic tumorigenicity. During phenotypic modulation, smooth muscle cells change their morphology, cell function and biochemical characteristics. Recent studies have focused on the regulation mechanism of smooth muscle cell-specific genes at the levels of transcription and/or alternative splicing in a phenotype-dependent manner. Typical examples of such genes include caldesmon, alpha-tropomyosin, myosin heavy chain, SM22, calponin and alpha 1 integrin. Cell adhesion molecules and growth factors/cytokines also play a critical role for controlling phenotype of smooth muscle cells via signal transduction pathways such as phosphoinositide 3-kinase and mitogen-activated protein kinases.
引用
收藏
页码:15 / 24
页数:10
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