Effect of liver receptor homolog-1 on cell apoptosis and steroid hormone secretion on granulosa cells from Hu sheep.

The apoptosis of granulosa cells can result in follicular atresia, a key process in follicle selection and development. The related molecular mechanisms were explored to study the effects of liver receptor homolog-1 (Lrh-1) on apoptosis, sodium-titanium system, and steroid synthesis of granulosa cells from Hu sheep in vitro. After constructing, designing, and synthesizing the Lrh-1 overexpression vector, liposomes were used to transfect Hu sheep granulosa cells. Thereafter, qRT-PCR and Western blot were used to detect the mechanism of Lrh-1 on the titanium system and steroid synthesis of Hu sheep granulosa cells. The overexpression efficiency was determined by fluorescence 48 h after liposome transfection into the Hu sheep granulosa cells in vitro culture. The transfection efficiency was higher, hence providing a basis for subsequent experiments. However, the protein level and transcriptional level of Lrh-1 significantly increased after transfection with Lrh-1 overexpression vector in Hu sheep granulosa cells. We further revealed that after Lrh-1 overexpression in Hu sheep granulosa cells, the expression of the pro-apoptotic gene Bax decreased significantly, while that of the anti-apoptotic gene Bcl-2 increased significantly, as well as the sodium peptide system. Moreover, the expression levels of natriuretic peptide precursor A, B, and C (NPPA, NPPB, NPPC) all showed an upward trend, while the expression levels of steroid synthesis-related genes (P450arom and P450scc) decreased. The above results showed that Lrh-1 overexpression influenced the apoptosis, sodium peptide system, and steroid synthesis.