Leukemia inhibitory factor prevents chicken follicular atresia through PI3K/AKT and Stat3 signaling pathways

Autophagy of granulosa cell (GC) may be a supplementary mechanism involved in follicular atresia through cooperating with apoptosis. Leukemia inhibitory factor (LIF) has been shown to promote follicular growth, through the underlying molecular mechanisms remain unclear. Rapamycin, an autophagy inducer, triggered the elevation of GC apoptosis within follicles, and then prevented follicular growth. However, combined treatment with LIF relieved the follicular regression caused by rapamycin, mainly resulting in alleviating the decline of GCs viability and cell autophagic apoptosis, and eventually, promoting follicle development. Further investigation revealed that LIF inhibited the GC autophagic apoptosis by activating PI3K/AKT and Stat3 pathways, reflecting an increase of BCL-2 expression but a decrease in BECN1. Additionally, blocking PI3K/AKT and Stat3 pathways resulted in the reduction of LIF protection against follicular atresia. These findings illustrated that LIF activated the PI3K/AKT and Stat3 signaling pathways to inhibit GC autophagic cell death, and further relieve chicken follicular atresia.

Automated summary

This study found that leukemia inhibitory factor (LIF) can inhibit autophagic cell death of granulosa cells by activating the PI3K/AKT and Stat3 signaling pathways, thus relieving granulosa cell apoptosis and promoting follicle development.