Effect of angiotensin II on pregnancy-associated plasma protein A and insulin-like growth factor 1 gene expression in human umbilical artery smooth muscle cells.
- Author:
Zheng ZHA
1
;
Qing-hua ZHANG
;
Zhi-xin JIANG
;
Ling CHEN
;
Hu LIN
;
Xue-mei LIANG
Author Information
- Publication Type:Journal Article
- MeSH: Angiotensin II; pharmacology; Cells, Cultured; Drug Synergism; Humans; Insulin-Like Growth Factor I; genetics; metabolism; Lipoproteins, LDL; pharmacology; Myocytes, Smooth Muscle; cytology; metabolism; Pregnancy-Associated Plasma Protein-A; genetics; metabolism; RNA, Messenger; genetics; metabolism; Umbilical Arteries; cytology; metabolism
- From: Journal of Southern Medical University 2009;29(2):195-198
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effect of angiotensin II (Ang II) on pregnancy-associated plasma protein A (PAPP-A) and insulin-like growth factor 1 (IGF-1) mRNA expressions in human umbilical artery smooth muscle cells (HUVSMCs).
METHODSIn the presence or absence of Ox-LDL, HUVSMCs were cultured with Ang II of 10(-5) mol/L for 0, 6, 12, 24, 36, and 48 h, or with Ang II at the concentrations of 10(-7), 10(-6), 10(-5), and 10(-4) mol/L for 24 h, after which the cells were then collected to detect PAPP-A and IGF-1 mRNA expressions in the cells using RT-PCR.
RESULTSAt the concentration of 10(-5) mol/L, Ang II showed a time-dependent effect in inducing PAPP-A and IGF-1 mRNA expressions, which began to increase at 12 h of culture and reaching the highest level at 24 h. Ang II also dose-dependently induced PAPP-A and IGF-1 mRNA expressions, and 10(-5) mol/L Ang II induced the highest expression levels of the two genes. Ox-LDL exposure significantly further increased the expression levels of PAPP-A and IGF-1 mRNA in the cells regardless of the Ang II concentration or duration for cell treatment (P<0.05).
CONCLUSIONAng II can time- and dose-dependently induces PAPP-A and IGF-1 mRNA expression in HUVSMCs and is responsible for inducing platelet activity and inflammatory reaction in acute coronary syndromes, and the effects of Ang II can be enhanced by Ox-LDL.
