The upregulation of TRPC6 contributes to Ca2+ signaling and actin assembly in human mesangial cells after chronic hypoxia
The upregulation of TRPC6 contributes to Ca2+ signaling and actin assembly in human mesangial cells after chronic hypoxia
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DOI：
10.1016/j.bbrc.2012.04.075
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发表时间：
2012-05-18
影响因子：
3.1
通讯作者：
Jiao, Jundong
中科院分区：
文献类型：
--
作者：
Liao, Chang;Yang, He;Jiao, Jundong
越来越多的证据表明系膜细胞是慢性缺氧损伤的重要靶点。受损的Ca2+信号被发现在系膜细胞（MCs）遭受慢性缺氧。然而，这一现象背后的机制尚未明确。在本研究中，我们发现慢性缺氧增强了TRPC6和TRPC6依赖性Ca2+进入的表达，TRPC6敲低抑制了慢性缺氧诱导的[Ca2+]i的增加，这表明TRPC6介导的Ca2+进入是MCs慢性缺氧诱导的[Ca2+]i升高的原因。此外，TRPC6敲低可减弱慢性缺氧诱导的肌动蛋白组装和肌动蛋白重组。我们得出结论，慢性缺氧后，TRPC6的上调参与了人MCs中Ca2+信号传导和肌动蛋白组装。这些发现为MCs对缺氧的细胞反应机制提供了新的见解。(C) 2012爱思唯尔公司版权所有。
There is increasing evidence that mesangial cells are important targets of chronic hypoxia injury. Impaired Ca2+ signaling has been found in mesangial cells (MCs) subjected to chronic hypoxia. However, the mechanisms underlying this phenomenon have not yet been defined. In the present study, we found that chronic hypoxia enhanced the expression of TRPC6 and TRPC6-dependent Ca2+ entry, and TRPC6 knockdown inhibited the chronic hypoxia-induced increase in [Ca2+]i, suggesting that TRPC6-mediated Ca2+ entry is responsible for the elevated [Ca2+]i induced by chronic hypoxia in MCs. In addition, TRPC6 knockdown attenuated chronic hypoxia-induced actin assembly and actin reorganization. We concluded that the upregulation of TRPC6 is involved in the Ca2+ signaling and actin assembly in human MCs after chronic hypoxia. These findings provide new insight into the mechanisms underlying the cellular response of MCs to hypoxia. (C) 2012 Elsevier Inc. All rights reserved.