Expression of 5-hydroxytamine receptors in hepatic stellate cell and action of 5-hydroxytamine on biological characteristics of hepatic stellate cell.
- Author:
Tao LI
1
;
Xi-sheng LENG
;
Shan-geng WENG
;
Ji-run PENG
;
Yu-hua WEI
;
Dong-cheng MOU
;
Wan-xiang WANG
;
Ji-ye ZHU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cells, Cultured; Hypertension, Portal; etiology; Liver; chemistry; cytology; Liver Cirrhosis; etiology; Male; Rats; Rats, Wistar; Receptors, Serotonin; analysis; physiology; Serotonin; pharmacology; Serotonin Antagonists; pharmacology; Transforming Growth Factor beta; physiology; Transforming Growth Factor beta1
- From: Chinese Journal of Surgery 2003;41(3):175-179
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the expression of 5-hydroxytamine receptors in hepatic stellate cells HSCs and action of 5-hydroxytamine on biological characteristics of HSC.
METHODSLiver ex vivo perfusion of collagenase and density gradient centrifugation were used to isolate hepatic stellate cell. RT-PCR was used to detect the expression of 5-hydroxytamine receptor subtypes 1A, 2A, 2B and 3. Western blot hybridization was used to elucidate the effect of 5-hydroxytamine and its 2A receptor antagonist ketanserin and 3 receptor antagonist ondanosetron on expression of transforming growth factor-beta1 (TGF-beta1) and Smad4 in HSC. HSCs were cultured on silicone membrane. The effect of 5-hydroxytamine, ketanserin and ondanosetron on cell contraction were studied.
RESULTSHSC expressed 5-hydroxytamine receptors subtypes 1A, 2A and 2B. 5-hydroxytamine significantly increased the expression of TGF-beta1 and Smad4 in HSC (P < 0.05). This was antagonized by ketanserin, not by ondanosetron. 5-hydroxytamine induced cell contraction in a dose-dependant manner. Ketanserin antagonized this action, but ondanosetron did not.
CONCLUSIONSHSCs express 5-hydroxytamine receptors. 5-hydroxytamine could affect the biological characteristics of HSC through its receptor mediation, and may play a role in the pathogenesis of liver cirrhosis and portal hypertension.
