Misárková E, Behuliak M, Bencze M, Zicha J
Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic.
Physiol Res. 2016 Jun 20;65(2):173-91. doi: 10.33549/physiolres.933317.
Vascular smooth muscle cells (VSMC) display considerable phenotype plasticity which can be studied in vivo on vascular remodeling which occurs during acute or chronic vascular injury. In differentiated cells, which represent contractile phenotype, there are characteristic rapid transient changes of intracellular Ca(2+) concentration ([Ca(2+)]i), while the resting cytosolic [Ca(2+)]i concentration is low. It is mainly caused by two components of the Ca(2+) signaling pathways: Ca(2+) entry via L-type voltage-dependent Ca(2+) channels and dynamic involvement of intracellular stores. Proliferative VSMC phenotype is characterized by long-lasting [Ca(2+)]i oscillations accompanied by sustained elevation of basal [Ca(2+)]i. During the switch from contractile to proliferative phenotype there is a general transition from voltage-dependent Ca(2+) entry to voltage-independent Ca(2+) entry into the cell. These changes are due to the altered gene expression which is dependent on specific transcription factors activated by various stimuli. It is an open question whether abnormal VSMC phenotype reported in rats with genetic hypertension (such as spontaneously hypertensive rats) might be partially caused by a shift from contractile to proliferative VSMC phenotype.
血管平滑肌细胞（VSMC）表现出相当大的表型可塑性，这可以在体内对急性或慢性血管损伤期间发生的血管重塑进行研究。在代表收缩表型的分化细胞中，细胞内Ca(2+)浓度（[Ca(2+)]i）有特征性的快速瞬时变化，而静息胞质[Ca(2+)]i浓度较低。这主要由Ca(2+)信号通路的两个成分引起：通过L型电压依赖性Ca(2+)通道的Ca(2+)内流和细胞内储存库的动态参与。增殖性VSMC表型的特征是[Ca(2+)]i持续振荡，同时基础[Ca(2+)]i持续升高。在从收缩表型向增殖表型转变的过程中，存在从电压依赖性Ca(2+)内流到非电压依赖性Ca(2+)内流进入细胞的总体转变。这些变化是由于基因表达改变所致，而基因表达改变取决于由各种刺激激活的特定转录因子。遗传性高血压大鼠（如自发性高血压大鼠）中报道的异常VSMC表型是否可能部分由从收缩性VSMC表型向增殖性VSMC表型的转变引起，这仍是一个悬而未决的问题。
