Effect of follicle-stimulating hormone and luteinizing hormone on apoptosis, autophagy, and the release and reception of some steroid hormones in yak granulosa cells through miR-23a/ASK1 axis

• Published in: Cellular signalling Vol. 115; p. 111010
• Main Authors: Xiao-Hong, Han, Meng, Wang, Yang-Yang, Pan, Jiang-Feng, Fan, Jing-Lei, Wang, Ling, Zhao, Ya-Ying, Wang, Tong-Xiang, Zhang, Tian, Zhao, Tian-Yi, Ding, Yan, Cui, Si-Jiu, Yu
• Format: Journal Article
• Language: English
• Published: England 01.03.2024
• Subjects: Animals; Apoptosis; Autophagy; Cattle; Estradiol - metabolism; Female; Follicle Stimulating Hormone - pharmacology; Follicular Atresia - physiology; Granulosa Cells - metabolism; Luteinizing Hormone - metabolism; Luteinizing Hormone - pharmacology; MAP Kinase Kinase Kinase 5 - metabolism; MicroRNAs - genetics; MicroRNAs - metabolism; Progesterone - metabolism; Granulosa cells; FSH and LH; miR-23a; Autophagy; ASK1; Apoptosis
• ISSN: 0898-6568; 1873-3913
• DOI: 10.1016/j.cellsig.2023.111010

Follicle-stimulating hormone (FSH), luteinizing hormone (LH), miR-23a, apoptosis signal-regulating kinase 1(ASK1)/c-Jun N-terminal kinase (JNK), autophagy and apoptosis play crucial roles in follicular development. However, their role in yak granulosa cells (GCs) remains unknown. Therefore, we examined the effect of miR-23a, ASK1, FSH, and LH on apoptosis, autophagy, and the release and reception of some steroid hormones in these cells. Our results showed that miR-23a overexpression significantly increased the abundance of Beclin1, the LC3II/I ratio, and the number of Ad-mRFP-GFP-LC3-labeled autophagosomes, and decreased p62 abundance. Additionally, Bax abundance and the number of terminal deoxynucleotidyl transferase deoxynucleotide triphosphate nick end labeling-positive cells were reduced, while Bcl2 expression was increased. Overexpression of miR-23a also significantly increased the abundance of estradiol receptor α (ER-α) and β (ER-β) and the concentrations of estradiol (E2), progesterone (P4) in yak GCs. Here, treating yak GCs with miR-23a decreased ASK1 expression, which regulates ASK1/JNK-mediated apoptosis, autophagy, E2 and P4 levels, and ER-α/β abundance. In contrast, treatment of yak GCs with FSH (10 μg/mL) and LH (100 μg/mL) increased miR-23a abundance, regulating the subsequent effect on ASK1/JNK-mediated apoptosis, autophagy, ER-α/β abundance, and E2 and P4 concentrations. In conclusion, miR-23a enhances autophagy in yak GCs, attenuates apoptosis, and increases ER-α/β abundance and E2 and P4 concentrations by downregulating ASK1. Additionally, FSH and LH can regulate these effects of miR-23a by altering its expression. These results provide important insights that can inform the development of strategies to reduce abnormal follicular atresia and improve the reproductive rate of yaks.