Lipopolysaccharide induces endothelial cell apoptosis via activation of Na⁺/H⁺ exchanger 1 and calpain-dependent degradation of Bcl-2

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• 作者：Yuxi Zhao ; Guimei Cui ; Nana Zhang ; Zengshan liu ; Wanchun Sun ; Qisheng Peng
• 关键词：Apoptosis ; Bcl-2 ; Endothelial cell ; Lipopolysaccharide ; Na+/H+ exchanger
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2012
• 出版时间：12 October, 2012
• 年：2012
• 卷：427
• 期：1
• 页码：125-132
• 全文大小：816 K

文摘

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 Ca²⁺ () 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 , which resulted in enhanced calpain activity as well as HUVECs apoptosis via NHE1-dependent degradation of Bcl-2.