Roles of SM22α in cellular plasticity and vascular diseases.
Roles of SM22α in cellular plasticity and vascular diseases.
复制标题
DOI：
10.2174/1871529x11202020119
复制
发表时间：
2012-11
期刊：
影响因子：
--
通讯作者：
Li-Hua Dong;Pin Lv;Mei Han
中科院分区：
文献类型：
--
作者：
Li-Hua Dong;Pin Lv;Mei Han
SM22α是钙钙蛋白家族中形状变化和转化敏感的22kda肌动蛋白结合蛋白。它普遍存在于血管和内脏平滑肌中，是平滑肌分化的早期标志。它也存在于成纤维细胞和一些上皮细胞中。SM22α可能参与不依赖钙的平滑肌收缩。最近的证据表明，SM22α的破坏可诱导血管炎症，并参与动脉疾病的骨软骨形成。这与NF-κB信号的激活是一致的，其中NF-κB活性在血管损伤中上调。高表达的SM22α抑制VSMCs和损伤动脉的细胞增殖。SM22α作为肿瘤抑制因子。它的表达缺失是细胞转化和某些肿瘤发展的早期事件，与细胞可塑性相一致。
SM22α is a shape change and transformation sensitive 22 kDa actin-binding protein of the calponin family. It is ubiquitous to vascular and visceral smooth muscle, and is an early marker of smooth muscle differentiation. It is also present in fibroblasts, and some epithelium. SM22α may be involved in calcium-independent smooth muscle contraction. Recent evidence suggests that disruption of SM22α induces vascular inflammation and is involved in osteochondrogenesis in arterial diseases. This is consistent with activation of NF-κB signaling, where NF-κB activity is upregulated in vascular injury. High expression of SM22α inhibits cell proliferation in VSMCs and in injured arteries. SM22α acts as a tumor suppressor. Loss of its expression is an early event in cell transformation and the development of some tumors, coinciding with cellular plasticity.