Does the miR-105–1-Kisspeptin Axis Promote Ovarian Cell Functions?

Abstract

AbstractThe objective of this study was to elucidate the intricate interplay among miR-105–1, kisspeptin, and their synergistic influence on basic ovarian granulosa cell functions. The effects of miR-105–1 mimics or miR-105–1 inhibitor, kisspeptin (0, 1, and 10 ng/ml), and its combinations with miR-105–1 mimics on porcine granulosa cells were assessed. The expression levels of miR-105–1, viability, proliferation (accumulation of PCNA, cyclin B1, XTT-, and BrdU-positive cells), apoptosis (accumulation of bcl-2, bax, caspase 3, p53, TUNEL-positive cells), proportion of kisspeptin-positive cells, and the release of steroid hormones and IGF-I were analyzed. Transfection of cells with miR-105–1 mimics promoted cell viability and proliferation, the occurrence of kisspeptin, and the release of progesterone and IGF-I; in contrast, miR-105–1 mimics inhibited apoptosis and estradiol output. MiR-105–1 inhibitor had the opposite effect. Kisspeptin amplified the expression of miR-105–1, cell viability, proliferation, steroid hormones, and IGF‐I release and reduced apoptosis. Furthermore, the collaborative action of miR-105–1 mimics and kisspeptin revealed a synergistic relationship wherein miR-105–1 mimics predominantly supported the actions of kisspeptin, while kisspeptin exhibited a dual role in modulating the effects of miR-105–1 mimics. These findings not only affirm the pivotal role of kisspeptin in regulating basic ovarian cell functions but also represent the inaugural evidence underscoring the significance of miR-105–1 in this regulatory framework. Additionally, our results show the ability of kisspeptin to promote miR-105–1 expression and the ability of miR‐105–1 to promote the occurrence and effects of kisspeptin and, therefore, indicate the existence of the self‐stimulating kisspeptin‐miR‐105–1 axis.