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Tumor necrosis factor‐α stimulates prostaglandin F2α secretion by bovine luteal cells via activation of mitogen‐activated protein kinase and phospholipase A2 pathways
Author(s) -
Sakumoto Ryosuke,
Murakami Shuko,
Okuda Kiyoshi
Publication year - 2000
Publication title -
molecular reproduction and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 105
eISSN - 1098-2795
pISSN - 1040-452X
DOI - 10.1002/1098-2795(200007)56:3<387::aid-mrd9>3.0.co;2-a
Subject(s) - biology , protein kinase a , secretion , mitogen activated protein kinase , microbiology and biotechnology , prostaglandin , phospholipase a2 , prostaglandin e2 , mapk/erk pathway , tumor necrosis factor alpha , kinase , medicine , endocrinology , mitogen activated protein kinase kinase , biochemistry , enzyme
It has been well demonstrated that tumor necrosis factor‐α (TNFα) stimulates prostaglandin (PG) F2α secretion by bovine corpus luteum (CL) in vitro. The objective of the present study was to clarify the intracellular signaling pathway of TNFα to stimulate PGF2α production in cultured bovine luteal cells. Bovine luteal cells that were obtained from mid‐ (days 8–12 after ovulation) CL were incubated with TNFα (0.6 nM) and/or various compounds as follows: U‐73122 (an inhibitor of phospholipase [PL] C), ACA (an inhibitor of PL‐A2), H‐89 (an inhibitor of protein kinase [PK] A), calphostin C (an inhibitor of PK‐C), L‐NAME/L‐NORG (inhibitors of nitric oxide synthase), and PD98059 (an inhibitor of mitogen‐activated protein kinase [MAPK] kinase). Although U‐73122 (0.1–10 μM), H‐89 (0.1–10 μM), calphostin C (0.01–1 μM) and L‐NAME/L‐NORG (1–100 μM) did not affect TNFα‐induced PGF2α secretion by the cultured cells, ACA (1–100 μM) and PD98059 (0.1–100 μM) inhibited TNFα‐stimulated PGF2α secretion by the cells in a dose‐dependent fashion ( P < 0.05 or lower). These findings suggest that TNFα activates the MAPK and PL‐A2 pathways in bovine luteal cells to stimulate PGF2α secretion. Mol. Reprod. Dev. 56:387–391, 2000. © 2000 Wiley‐Liss, Inc.