Effect of sex hormones on heme oxygenase expression in rat ventral prostate.
- Author:
Jian TIAN
1
;
Yu ZHENG
;
Chun YANG
Author Information
1. Department of Physiology, West China School of Preclinical and Forensic Medicine of Sichuan University, Chengdu 610044, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Carbon Monoxide;
metabolism;
Heme Oxygenase (Decyclizing);
biosynthesis;
genetics;
Heme Oxygenase-1;
Male;
Orchiectomy;
Prostate;
enzymology;
metabolism;
RNA, Messenger;
biosynthesis;
genetics;
Random Allocation;
Rats;
Rats, Sprague-Dawley;
Testosterone Propionate;
pharmacology
- From:
Acta Physiologica Sinica
2004;56(1):54-59
- CountryChina
- Language:Chinese
-
Abstract:
Heme oxygenase (HO) is a rate-limiting enzyme for endogenous carbon monoxide (CO) production. Recently it has been suggested that endogenous CO plays an important role in regulating smooth muscle tone. The development of bladder outlet obstruction in men with benign prostates hyperplasia was shown to be related to the prostates smooth muscle tone, but it was not clear whether endogenous HO/CO system mediates prostates smooth muscle activity. To investigate the influence of sex hormone on the expression of heme oxygenase (HO) gene in rat ventral prostate, we created the model of castrated male rats to test the mRNA levels of HO-1 and HO-2 by RT-PCR, and used immunohistochemical staining procedures with image analytic technical system to confirm the effects of exogenous androgen and estrogen on the expression of HO-1 and HO-2 protein in rat ventral prostate. The results showed that two isoforms of HO were present in rat ventral prostate. The epithelial cells of acini and fibromuscular stroma of the rat prostate displayed HO-1 immunoreactivity, whereas HO-2 immunostaining was only examined to be in the acinar cells. Both at protein and transcript levels, HO-1 in castrated group was markedly decreased compared with the normal control group (p<0.01). In groups of exogenous administration of androgen and estrogen HO-1 was much higher than that in the control groups (p<0.01). However, estrogen increased HO-1 protein level in prostate stroma, while the levels of HO-2 did not give any evidence of change among all groups (p>0.05). These findings suggest that expression of HO-1 gene is induced by sex hormones, in contrast, there is no change in HO-2 expression. We speculate that CO-HO system is possibly involved in the pathologic processes of prostates abnormal proliferation induced by sex hormones and that CO derived from HO-1 may play an important role in the regulation of smooth muscle activity in rat prostate.
