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PTPN5 promotes follicle‐stimulating hormone secretion through regulating intracellular calcium homeostasis
Author(s) -
Wang Hongmei,
Bu Siyuan,
Tang Jiajian,
Li Yi,
Liu Chunhua,
Dong Junhong
Publication year - 2021
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.202002752rr
Subject(s) - gonadotropic cell , medicine , endocrinology , microbiology and biotechnology , biology , follicle stimulating hormone , protein tyrosine phosphatase , phosphatase , luteinizing hormone , secretion , chemistry , phosphorylation , hormone
Abstract Protein tyrosine phosphatase non‐receptor type 5 (PTPN5), also called striatal‐enriched protein tyrosine phosphatase (STEP), is highly expressed in neurons of the basal ganglia, hippocampus, cortex, and related structures, also in the pituitary. Gonadotropins are the key regulator of the reproduction in mammals. In this study, PTPN5 is detected to express in murine pituitary in a developmental manner. Moreover, the expression of PTPN5 in the pituitary is heavily reduced after ovary removal. Follicle‐stimulating hormone (FSH) secretion in gonadotropes is regulated by PTPN5 via binding GnRH to GnRH‐R. Two parallel signaling pathways, Gs‐protein kinase A (PKA)‐PTPN5 and Gq‐phospholipases C (PLC)‐p38 MAPK‐PTPN5, cooperatively regulate GnRH‐induced FSH secretion. We also show that influx of Ca 2+ activates the Ca 2+ ‐dependent phosphatase calcineurin, leading to the phosphorylation and activation of PTPN5. The intracellular release of Ca 2+ is reduced via TC2153. In conclusion, blocking or knocking out of PTPN5 reduces the release of FSH in whole pituitary. Mechanically, PTPN5 regulates gonadotropes' function through regulating intracellular calcium homeostasis.