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首页> 外文期刊>Journal of Cellular Physiology >Smooth muscle phenotypic diversity is mediated through alterations in myocardin gene splicing.
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Smooth muscle phenotypic diversity is mediated through alterations in myocardin gene splicing.

机译：平滑肌表型多样性是介导通过改变myocardin基因拼接。

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摘要

Myocardin (MYOCD) is a smooth and cardiac muscle-specific transcriptional coactivator that is required for the proper expression of contraction-related genes. Through its function to transactivate effector genes, MYOCD plays an essential role in mediating the switch between contractile and non-contractile phenotypes, particularly in smooth muscle cells (SMC). There are at least two known transcript variants of MYOCD that are expressed in SMC, differing only by the presence (+) or absence (Delta) of Exon 11. To date, no functional role has been assigned to the domain encoded by Exon 11, nor have any notable differences between the ability of each isoform to activate contraction-related genes been observed. In this study we compared sequences for Exon 11 among several mammalian species and identified a highly conserved, putative target sequence for glycogen synthase kinase 3 (GSK3) phosphorylation, suggesting a regulatory role for Exon 11 that can be modulated by alternative splicing. The function of Exon 11 was investigated by altering MYOCD splice selection in cultured porcine SMC with small interfering RNAs (siRNA) and specific chemical inhibitors, resulting in a relative increase in expression of DeltaExon 11 variants in the endogenous pool of MYOCD mRNA. The relative increase in DeltaExon 11 mRNAs correlated with a reduction of contractile phenotype in the porcine SMC as evidenced by morphological assessment and molecular analysis of effector genes. Together, these data suggest that MYOCD DeltaExon 11 may participate in modulating SMC phenotype, potentially acting as a dominant-negative repressor of contraction-related genes.
机译：Myocardin (MYOCD)是一个光滑的和心脏阳性转录共激活剂,需要适当的表达吗contraction-related基因。MYOCD扮演transactivate效应基因在调节之间切换的重要作用收缩和non-contractile表型,尤其是在平滑肌细胞(SMC)。至少有两个已知的转录变异MYOCD用SMC表示,不同的(+)或外显子缺失(δ)11. 域由外显子编码11,也没有任何显著差异的能力同种型激活contraction-related基因被观察到。对第11外显子序列数哺乳动物物种和确定一个高度保守的,假定的目标序列糖原合酶激酶3 (GSK3)磷酸化,暗示监管角色外显子11可以调制可变剪接。研究了通过改变MYOCD拼接选择培养猪SMC用小干扰rna (siRNA)和特定的化学物质抑制剂,导致相对增加表达DeltaExon 11的变体内源性MYOCD信使rna。DeltaExon 11 mrna与增加减少收缩表型的猪SMC形态学评估,就证明了这一点效应基因的分子分析。这些数据表明,MYOCD DeltaExon 5月11日参与调节SMC表型,可能作为显性负contraction-related基因的抑制因子。

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