Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 427, Issue 1, Pages 125-132Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2012.09.023
Keywords
Apoptosis; Bcl-2; Endothelial cell; Lipopolysaccharide; Na+/H(+)exchanger
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Funding
- Jilin University [450060445662, 430504001043, 430505010272]
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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+ (Ca-j(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-j(2+), which resulted in enhanced calpain activity as well as HUVECs apoptosis via NHE1-dependent degradation of Bcl-2. (C) 2012 Elsevier Inc. All rights reserved.
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