Expression and role of resistin on steroid secretion in the porcine corpus luteum

Author:

Kurowska Patrycja1,Sroka Monika1,Dawid Monika1,Mlyczyńska Ewa1,Respekta Natalia1,Jurek Małgorzata1,Klimczyk Dominika1,Grzesiak Małgorzata2,Dupont Joelle3,Rak Agnieszka1ORCID

Affiliation:

1. 1Laboratory of Physiology and Toxicology of Reproduction, Institute of Zoology and Biomedical Research, Jagiellonian University in Krakow, Krakow, Poland

2. 2Department of Endocrinology, Institute of Zoology and Biomedical Research, Jagiellonian University in Krakow, Krakow, Poland

3. 3INRAE, UMR85, Unité Physiologie de la Reproduction et des Comportements, Nouzilly, France

Abstract

Resistin plays an important role in adipogenesis, obesity, insulin resistance, and reproduction. Previous studies showed resistin action on ovarian follicular cells; however, whether resistin regulates steroid secretion in luteal cells is still unknown. Our aim was first to determine the expression of resistin and its potential receptors (tyrosine kinase-like orphan receptor 1 (ROR1) and toll-like receptor 4 (TLR4)) in the porcine corpus luteum (CL), regulation of its expression, effect on kinases phosphorylation, and luteal steroidogenesis. Our results showed that the expression of resistin and its receptors was dependent on the luteal phase and this was higher at the mRNA level in the late compared with the early and middle luteal phase. At the opposite, resistin protein expression was higher in the middle and late compared with the early luteal phase, while ROR1 and TLR4 expression was highest in the early luteal phase. Additionally, we observed cytoplasmic localisation of resistin, ROR1, and TLR4 in small and large luteal cells. We found that luteinising hormone, progesterone (P4), insulin, and insulin-like growth factor 1 regulated the protein level of resistin, ROR1, and TLR4. Resistin decreased P4 and increased oestradiol (E2) secretion via changes in steroidogenic enzymes expression and via the activation of protein kinase A (PKA) and mitogen-activated protein kinase (MAP3/1), increased the expression of receptors LHCGR and ESR2 and decreased the expression of PGR. Moreover, resistin decreased PKA phosphorylation and enhanced MAP3/1 phosphorylation. Taken together, resistin could act directly on steroid synthesis and serve as an important factor in in vivo luteal cell function.

Publisher

Bioscientifica

Subject

Cell Biology,Obstetrics and Gynecology,Endocrinology,Embryology,Reproductive Medicine

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