Gonadotropin-inhibiting hormone promotes apoptosis of bovine ovary granulosa cells

Gonadotropin-inhibiting hormone (GnIH) inhibits the synthesis and release of gonadotropin by binding to its receptor. GnIH is involved in animal reproductive regulation, especially ovary function. It can regulate the proliferation, apoptosis and hormone secretion of follicular cells. However, the role and molecular mechanism of GnIH in bovine granulosa cell (bGC) apoptosis is unclear. Here, the effects of GnIH on proliferation, apoptosis, and mitochondrial function of bGCs were detected. A 10(-6) mol/mL concentration of GnIH inhibited bGC proliferation, promoted GC apoptosis, and damaged mitochondrial function. Additionally, GnIH significantly decreased the phosphorylation level of p38 (P < 0.01). To explore the role of the p38 signaling pathway in the process of GnIH-induced apoptosis in bGCs, an activator of p38 (U46619) was used to pretreat bGCs. U46619 pretreatment significantly alleviated GnIH damage to bGCs, including proliferation, apoptosis, and mitochondrial function. In conclusion, these results demonstrated that GnIH inhibited proliferation and promoted apoptosis of bGCs via the p38 signaling pathway.

Automated summary

Research indicates that GnIH inhibits the proliferation and promotes apoptosis of bovine granulosa cells through the p38 signaling pathway, and the use of a p38 activator can alleviate these effects.