Angiotensin Ⅱ promotes NO production, inhibits apoptosis and enhances adhesion potential of bone marrow-derived endothelial progenitor cells

• 来源期刊: 细胞研究（英文版）
• 年，卷（期）: 2008,（7）
• 页码范围: 792-799
• 页数: 8页
• 语种: 英文

摘要

Endothelial progenitor cells (EPCs) participate in the processes of postnatal neovascularization and re-endothelialization in response to tissue ischemia and endothelial injury. The level of EPCs present has been found to be directly associated with the outcome of cardiovascular diseases, and could be regulated by stimulatory or inhibitory factors. Given the close relationship between angiotensin Ⅱ (Angll) and the cardiovascular system, we investigated the effect of Angll on the activities of bone marrow (BM)-derived EPCs. Cells were isolated from BM of rats by density gradient centrifugation. Administration of Angll significantly promoted nitric oxide (NO) release, inhibited EPC apoptosis and enhanced EPC adhesion potential. All of these Angll-mediated effects on EPCs were attenuated by pretreatment with valsartan or L-NAME. Moreover, both LY294002 and wortmannin abolished the anti-apoptotic effect of Angll. Western blot analyses indicated that endothelial NO synthase (eNOS) protein and phosphorylated Akt increased with the treatment of Angll in EPCs. Thus, Angll improved several activities of EPCs through Angll type 1 receptor (ATIR), which may represent a possible mechanism linking Angll and ATlR with angiogenesis. Additionally, Angll-induced NO synthesis through eNOS in EPCs regulates apoptosis and adhesion, and the PI3-kinase/Akt pathway has an essential role in Angll-induced antiapoptosis signaling.