Key Laboratory for Zoonosis Research, Ministry of Education, Institute of Zoonosis, Jilin University, Changchun 130062, People's Republic of China.
Biochem Biophys Res Commun. 2012 Oct 12;427(1):125-32. doi: 10.1016/j.bbrc.2012.09.023. Epub 2012 Sep 17.
The calcium-dependent protease calpain is involved in lipopolysaccharide (LPS)-induced endothelial injury. The activation of Na(+)/H(+) exchanger (NHE) is responsible to increase intracellular Ca(2+) (Ca(i)(2+)) in cardiovascular diseases. Here we hypothesized that activation of NHE mediates LPS-induced endothelial cell apoptosis via calcium-dependent calpain pathway. Our results revealed that LPS-induced increases in NHE activity are dependent on NHE1 in human umbilical vein endothelial cells (HUVECs). Treatment of HUVECs with LPS increased the NHE1 activity in a time-dependent manner associated with the increased Ca(i)(2+), which resulted in enhanced calpain activity as well as HUVECs apoptosis via NHE1-dependent degradation of Bcl-2.
钙依赖性蛋白酶钙蛋白酶参与脂多糖 (LPS) 诱导的内皮细胞损伤。Na(+)/H(+) 交换器 (NHE) 的激活负责增加心血管疾病中的细胞内 Ca(2+) (Ca(i)(2+))。在这里，我们假设 NHE 的激活通过钙依赖性钙蛋白酶途径介导 LPS 诱导的内皮细胞凋亡。我们的结果表明，LPS 诱导的 NHE 活性增加依赖于人脐静脉内皮细胞 (HUVEC) 中的 NHE1。LPS 处理 HUVEC 会导致 NHE1 活性呈时间依赖性增加，同时 Ca(i)(2+) 增加，导致钙蛋白酶活性增强，以及通过 NHE1 依赖性 Bcl-2 降解导致 HUVEC 凋亡。
