G protein-coupled estrogen receptor promotes acrosome reaction via regulation of Ca2+ signaling in mouse sperm

G protein-coupled estrogen receptor (GPER), a seven-transmembrane G protein-coupled receptor, mediates the rapid pre-genomic signaling actions of estrogen and derivatives thereof. The expression of GPER is extensive in mammal male reproductive system. However, the functional role of GPER in mouse sp...

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Published inBiology of reproduction Vol. 107; no. 4; pp. 1026 - 1034
Main Authors Gao, Dong-Dong, Lan, Chong-Feng, Cao, Xiao-Nian, Chen, Lei, Lei, Tian-Lun, Peng, Lei, Xu, Jia-Wen, Qiu, Zhuo-Er, Wang, Long-Long, Sun, Qing, Huang, Zi-Yang, Zhu, Yun-Xin, Zhou, Wen-Liang, Zhang, Yi-Lin
Format Journal Article
LanguageEnglish
Published Cary Society for the Study of Reproduction 11.10.2022
Oxford University Press
Subjects
17β-Estradiol
Acrosome reaction
Ca2+ signaling
Calcium (intracellular)
Calcium influx
Calcium signalling
CatSper
Chlortetracycline
Estrogen receptors
Estrogens
Flagella
GPER
IP3R
Phospholipase C
PLC
Proteins
Reproductive system
RESEARCH ARTICLE
Sperm
CatSper
R
signaling
PLC
GPER
IP
acrosome reaction
Ca
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Summary:G protein-coupled estrogen receptor (GPER), a seven-transmembrane G protein-coupled receptor, mediates the rapid pre-genomic signaling actions of estrogen and derivatives thereof. The expression of GPER is extensive in mammal male reproductive system. However, the functional role of GPER in mouse sperm has not yet been well recognized. This study revealed that GPER was expressed at the acrosome and the mid-flagellum of the mouse sperm. The endogenous GPER ligand 17β-estradiol and the selective GPER agonist G1 increased intracellular Ca2+ concentration ([Ca2+]i) in mouse sperm, which could be abolished by G15, an antagonist of GPER. In addition, the G1-stimulated Ca2+ response was attenuated by interference with the phospholipase C (PLC) signaling pathways or by blocking the cation channel of sperm (CatSper). Chlortetracycline staining assay showed that the activation of GPER increased the incidence of acrosome-reacted sperm. Conclusively, GPER was located at the acrosome and mid-flagellum of the mouse sperm. Activation of GPER triggered the elevation of [Ca2+]i through PLC-dependent Ca2+ mobilization and CatSper-mediated Ca2+ influx, which promoted the acrosome reaction of mouse sperm. Graphical Abstract
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ISSN:0006-3363
1529-7268
DOI:10.1093/biolre/ioac136