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Functional expression of G protein‐coupled receptor 30 in immature rat epididymal epithelium
Author(s) -
Cao Xiaonian,
Huang Jiehong,
Zhang Geng,
Zuo Wulin,
Lan Chongfeng,
Sun Qing,
Yang Dengliang,
Gao Dongdong,
Cheng Christopher H.K.,
Zhou WenLiang
Publication year - 2017
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10709
Subject(s) - epididymis , gper , microbiology and biotechnology , endocrinology , medicine , epithelium , receptor , biology , agonist , chloride channel , chemistry , biochemistry , estrogen receptor , sperm , breast cancer , botany , genetics , cancer
The aim of this study is to investigate the functional role of G protein‐coupled receptor 30 (GPR30) in the epididymis. We found that GPR30 is expressed in the epithelium of the immature rat epididymis and is involved in chloride secretion into the caudal epididymis lumen. The short‐circuit current (Isc) experiments showed that in primary cultured caudal epididymis epithelium, activation of GPR30 by its specific agonist G1 induced a mono‐phasic current increase, and G15, the specific antagonist of GPR30, could completely inhibit the current induced by G1. The G1‐induced Isc was largely blocked by application of the non‐specific chloride channel inhibitor diphenylamine‐dicarboxylic acid (DPC), or by the cystic fibrosis transmembrane conductance regulator (CFTR) inhibitor CFTR inh‐172 , suggesting that the current was mainly mediated through CFTR. In addition, after stimulating GPR30 by G1, the intracellular concentration of cAMP in the epithelium was significantly increased, indicating that the cAMP signal pathway is involved and could be responsible for the CFTR activation. Finally, to further investigate the function of GPR30 in vivo, G15 was administrated into rats subcutaneously. The osmotic pressure of the micro perfusion solution from epididymis was measured and the sperms were collected. Results showed that there was an osmotic pressure increase of the perfusion solution from G15 treated rats. When the GPR30 was inhibited by G15 endogenously, the motility of sperms decreased. Our data demonstrated that GPR30 is involved in the formation of caudal epididymis fluid micro‐environment thus affecting sperm motility.