Role of insulin-like growth factor-1 (IGF-1) in regulating cell cycle progression.
Role of insulin-like growth factor-1 (IGF-1) in regulating cell cycle progression.
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DOI：
10.1016/j.bbrc.2009.08.114
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发表时间：
2009-11
影响因子：
3.1
通讯作者：
Q. Ma;Tian-lun Yang;J. Yin;Z. Peng;Min Yu;Zhaoqian Liu;Fang-Ping Chen
中科院分区：
文献类型：
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作者：
Q. Ma;Tian-lun Yang;J. Yin;Z. Peng;Min Yu;Zhaoqian Liu;Fang-Ping Chen
AIMSInsulin-like growth factor-1 (IGF-1) is a polypeptide protein hormone, similar in molecular structure to insulin, which plays an important role in cell migration, cell cycle progression, cell survival and proliferation. In this study, we investigated the possible mechanisms of IGF-1 mediated cell cycle redistribution and apoptosis of vascular endothelial cells.METHODHuman umbilical vein endothelial cells (HUVECs) were pretreated with 0.1, 0.5, or 2.5μg/mL of IGF-1 for 30min before the addition of Ang II. Cell cycle redistribution and apoptosis were examined by flow cytometry. Expression of Ang II type 1 (AT1) mRNA and cyclin E protein were determined by RT-PCR and Western blot, respectively.RESULTSAng II (1μmol/L) induced HUVECs arrested at G0/G1, enhanced the expression level of AT1mRNA in a time-dependent manner, reduced the enzymatic activity of nitric oxide synthase (NOS) and nitric oxide (NO) content as well as the expression level of cyclin E protein. However, IGF-1 enhanced NOS activity, NO content, and the expression level of cyclin E protein, and reduced the expression level of AT1mRNA. L-NAME significantly counteracted these effects of IGF-1.CONCLUSIONSOur data suggests that IGF-1 can reverse vascular endothelial cells arrested at G0/G1and apoptosis induced by Ang II, which might be mediated via a NOS–NO signaling pathway and is likely associated with the expression levels of AT1 mRNA and cyclin E proteins.
