Luteal fibroblasts produce prostaglandins in response to IL1β in a MAPK-mediated manner.

Autor: Monaco CF; Department of Obstetrics and Gynecology, University of Nebraska Medical Center, Omaha, NE, USA; Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE, USA., Jones CM; Department of Obstetrics and Gynecology, University of Nebraska Medical Center, Omaha, NE, USA., Sayles HR; Department of Biostatistics, College of Public Health, University of Nebraska Medical Center, Omaha, NE, USA., Rudloff B; Department of Animal Science, University of Nebraska-Lincoln, Lincoln, NE, USA., McFee R; Department of Animal Science, University of Nebraska-Lincoln, Lincoln, NE, USA., Cupp AS; Department of Animal Science, University of Nebraska-Lincoln, Lincoln, NE, USA., Davis JS; Department of Obstetrics and Gynecology, University of Nebraska Medical Center, Omaha, NE, USA; US Department of Veterans Affairs VA Medical Center, Omaha, NE, USA. Electronic address: jsdavis@unmc.edu.
Jazyk: angličtina
Zdroj: Molecular and cellular endocrinology [Mol Cell Endocrinol] 2025 Jan 15; Vol. 596, pp. 112420. Date of Electronic Publication: 2024 Nov 25.
DOI: 10.1016/j.mce.2024.112420
Abstrakt: The corpus luteum is a temporary endocrine gland that is crucial for pregnancy, as it produces the progesterone needed to maintain optimal uterine conditions for implantation. In the absence of a conceptus, the corpus luteum becomes non-functional and undergoes rapid tissue remodeling to regress into a fibrotic corpus albicans. Early luteal regression is characterized by increased cytokine release. Because the role of fibroblasts in the bovine corpus luteum remains to be elucidated, the aim of this study was to elucidate the response of bovine luteal fibroblasts to inflammatory cytokines, tumor necrosis factor α (TNFα), and interleukin 1β (IL1β). Both cytokines induced canonical mitogen activated protein kinase (MAPK) signaling in luteal fibroblasts by phosphorylation of ERK1/2, p38 MAPK, and JNK. IL1β elevated expression and phosphorylation of cytosolic phospholipase A2 (cPLA 2 ), an enzyme that mobilizes arachidonic acid for prostanoid synthesis. IL1β also elevated expression of prostaglandin-endoperoxide synthase 2 (PTGS2), another enzyme needed to synthesize prostanoids. IL1β increased PGF2α and PGE 2 levels in the culture medium over 20-fold. Inhibition of MAPKs with small-molecule inhibitors abrogated the stimulatory effects of IL1β. IL1β also induced prostaglandin production in steroidogenic cells; however, there was no elevation in cPLA 2 . Therefore, actions of IL1β differ based on ovarian cell type. All together, we have identified luteal fibroblasts as potential inflammatory mediators during luteal regression.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Published by Elsevier B.V.)
Databáze: MEDLINE
Externí odkaz: