Study on the mechanism of how vasonatrin peptide can attenuate the growth-promoting effect of hypoxia in cardiac fibroblasts.
- Author:
Jun YU
1
;
Miao-Zhang ZHU
;
Bao-Ying CHENG
;
Shun-Yan LU
;
Ming-Qing DONG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Animals, Newborn; Atrial Natriuretic Factor; pharmacology; Cell Hypoxia; Cells, Cultured; Cyclic GMP; metabolism; Myoblasts, Cardiac; cytology; drug effects; Proliferating Cell Nuclear Antigen; metabolism; Rats; Rats, Sprague-Dawley
- From: Chinese Journal of Applied Physiology 2003;19(1):8-11
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo investigate how vasonatrin peptide (VNP) can attenuate the growth-promoting effect of hypoxia in cardiac fibroblasts cultured from neonatal rats.
METHODSThe cultured cardiac fibroblasts were divided randomly into four groups: control group, hypoxia group, hypoxia + VNP group and hypoxia + 8-Bromo-cGMP group. The growth of cardiac myocytes was measured by the means of MTT method. The effect of VNP on the intracellular level of cGMP and PCNA were measured by the means of radioimmunoassay and immunohistochemistry stain respectively.
RESULTSHypoxia (24 h) significantly increased the MTT A490nm value of cardiac fibroblasts (P < 0.05 vs control group). Both VNP (10(-7) mol/L) and 8-Bromo-cGMP (10(-3) mol/L) decreased MTT A490 nm value in cardiac fibroblast (P < 0.05 vs hypoxia group). VNP (10(-7) mol/L) increased the intracellular level of cGMP (P < 0.05 vs control and hypoxia group). Hypoxia (24 h) significantly increased the expression of proliferating cell nuclear antigen (PCNA) in cardiac myocytes (P < 0.05, vs control group), but VNP (10(-7) mol/L) decreased it.
CONCLUSIONVNP can attenuate hypoxia-induced growth-promoting effect in cardiac fibroblasts which is associated with the changes of cGMP and PCNA.
