TRPM7 channel regulates ox-LDL-induced proliferation and migration of vascular smooth muscle cells via MEK-ERK pathways
TRPM7 channel regulates ox-LDL-induced proliferation and migration of vascular smooth muscle cells via MEK-ERK pathways
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DOI：
10.1002/1873-3468.12088
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发表时间：
2016-02-01
期刊：
影响因子：
3.5
通讯作者：
Zhang, Liming
中科院分区：
文献类型：
--
作者：
Lin, Jinghan;Zhou, Shanshan;Zhang, Liming
瞬时受体电位melastatin 7（TRPM 7）在多种细胞类型的病理生理反应中起关键作用。然而，TRPM 7通道在ox-LDL诱导的VSMC增殖和迁移中的作用尚不清楚。本研究以胸主动脉VSMCs为研究对象，探讨ox-LDL对VSMCs增殖和迁移的影响，并探讨其分子机制和信号通路。结果表明，ox-LDL可显著增加TRPM 7活性，诱导VSMC增殖和迁移。非特异性TRPM 7阻断剂2-APB或靶向TRPM 7的合成siRNA抑制VSMC增殖和迁移。此外，与细胞增殖和迁移相关的ERK 1/2和MEK 1/2的磷酸化在TRPM 7缺陷的VSMC中减少。因此，TRPM 7可能构成治疗动脉粥样硬化的有用靶点。
Transient receptor potential melastatin 7 (TRPM7) plays a key role in the pathophysiological response of multiple cell types. However, the role of TRPM7 channels in ox-LDL-induced proliferation and migration of VSMC remains unclear. This study used the thoracic aorta VSMCs to explore the effects of ox-LDL on cell proliferation and migration and to investigate the underlying molecular mechanisms and signaling pathways. Data demonstrated that ox-LDL significantly increased TRPM7 activity, and induced VSMC proliferation and migration. VSMC proliferation and migration were inhibited by nonspecific TRPM7 blocker 2-APB or synthetic siRNA targeting TRPM7. Furthermore, the phosphorylation of ERK1/2 and MEK1/2 associated with cell proliferation and migration decreased in TRPM7-deficient VSMC. Therefore, TRPM7 may constitute a useful target for the treatment of atherosclerosis.