An experimental study on the regulation of pulmonary arterial remodeling by protein kinase C in chronic hypoxic rats.
- Author:
Hao ZHOU
1
;
Shao-Xian CHEN
;
Liang-Xing WANG
;
Yan-Fan CHEN
;
Yu-Peng XIE
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Collagen; metabolism; Female; Hypertension, Pulmonary; metabolism; physiopathology; Hypoxia; metabolism; physiopathology; Male; Myocytes, Smooth Muscle; metabolism; Protein Kinase C; metabolism; Pulmonary Artery; physiopathology; Rats; Rats, Sprague-Dawley
- From: Chinese Journal of Applied Physiology 2002;18(1):38-42
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo investigate the effect of protein kinase C regulating pulmonary arterial remodeling in chronic hypoxic rats.
METHODSElectron microscope, radioactivity, immunohistochemistry and image analyser were used.
RESULTS(1) Mean pulmonary arterial pressure (mPAP) and weight ratio of RV to LV + S were significantly higher than that of control group (P < 0.01). (2) WA/TA and SMC were significantly higher than that of control group (P < 0.01). Electron microscopy showed the proliferation of smooth muscle cells and the disposition of collagenous fiber in pulmonary arterioles induced by hypoxia. (3) The total, cytosolic, particulate fraction PKC activity and the ratio of particulate fraction to total PKC activity were significantly higher than that of control group (P < 0.01). (4) Expression of PKC, collagen I were significantly higher than that of control group (P < 0.01), the difference of collagen III was not significant between two groups (P > 0.05). (5) There were good correlation between the total, particulate fraction PKC activity, the ratio of particulate fraction to total PKC activity, expression of PKC and SMC, collagen I in pulmonary arterioles.
CONCLUSIONThe PKC regulates the proliferation of pulmonary artery smooth muscle cells and expression of pulmonary arterial collagen in chronic hypoxic rats, which may play an important role in the pathogenesis of pulmonary hypertension and structural remodeling of pulmonary arteries.