当前位置： SCI文献检索 > BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS期刊下所有文献 > 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.

Abstract：

AIMS:Insulin-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. METHOD:Human umbilical vein endothelial cells (HUVECs) were pretreated with 0.1, 0.5, or 2.5 microg/mL of IGF-1 for 30 min before the addition of Ang II. Cell cycle redistribution and apoptosis were examined by flow cytometry. Expression of Ang II type 1 (AT(1)) mRNA and cyclin E protein were determined by RT-PCR and Western blot, respectively. RESULTS:Ang II (1 micromol/L) induced HUVECs arrested at G(0)/G(1), enhanced the expression level of AT(1) mRNA 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 AT(1) mRNA. L-NAME significantly counteracted these effects of IGF-1. CONCLUSIONS:Our data suggests that IGF-1 can reverse vascular endothelial cells arrested at G(0)/G(1) and 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.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Ma QL,Yang TL,Yin JY,Peng ZY,Yu M,Liu ZQ,Chen FP

doi

10.1016/j.bbrc.2009.08.114

subject

Has Abstract

pub_date

2009-11-06 00:00:00

pages

150-5

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(09)01705-7

journal_volume

389

pub_type

杂志文章

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