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CELL MEMBRANE GPER AND ERα ON MYOMETRIUM: TWO DISTINCT RECEPTORS WITH DISTINCT SIGNALLING PATHWAYS

OANA SORINA TICA1, ELENA DELIU2, TUDOREL CIUREA3,4, XIN GAO5, ANA-MARIA BUGA6,7, EUGEN OSIAC6,8, DRAGOS ALEXANDRU6,9, ANDREI ADRIAN TICA6,10*

1.Department of Mother and Child, University of Medicine and Pharmacy of Craiova, Romania
2 .Department of Pharmacology, School of Medicine, Temple University of Philadelphia, USA
3 .Research Centre of Gastroenterology and Hepatology, University of Medicine and Pharmacy of Craiova, Romania
4 .Gastroenterology Department, University of Medicine and Pharmacy of Craiova, Romania
5 .Neuroinflammation DPU GSK R&D, Shanghai, China
6 .Research Centre for Clinical and Experimental Medicine, University of Medicine and Pharmacy of Craiova, Romania
7 .Biochemistry Department, University of Medicine and Pharmacy of Craiova, Romania
8 .Biophysics Department, University of Medicine and Pharmacy of Craiova, Romania
9 .Biostatistics Department, University of Medicine and Pharmacy of Craiova, Romania
10 .Pharmacology Department, University of Medicine and Pharmacy of Craiova, Romania

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he “rapid” effects of oestrogens on myometrium mainly result by activating cell membrane oestrogen receptors: ERα and GPER (G protein coupled oestrogen receptor 1). In contrast to the contractile effect induced by G-1 (GPER agonist), effect involving the opening of L-type calcium channels, oestradiol (E2) inhibited until arrest the spontaneous contractile activity and significantly decreased the contraction induced by high K+ or oxytocin. The effects of E2 were not blocked by G-15 (GPER antagonist). We concluded that the “rapid” effects E2-induced on myometrium are the result of cell membrane ERα activation and mainly consist of the inhibition of L-type calcium channels. It is a sticking difference between the genomic and non-genomic effect of E2 on oxytocin-induced signalling pathway. Finally, it is very probable a masking/inhibition (modulator) effect of ERα on cell membrane GPER activity.