Host: Society for Reproduction and Development
[Introduction] Progesterone (P4) has been demonstrated to be an anti-apoptotic agent in bovine luteal steroidogenic cells (LSC). Since luteinizing hormone (LH) is one of the most potent stimulators of P4 production by the corpus luteum (CL), we hypothesized that LH suppresses apoptosis of LSC via P4. To confirm the above hypothesis, we examined the effect of LH on cell death and expression of apoptosis related proteins in LSC. [Materials and Methods] Cultured bovine LSC at the mid stage were treated for 24 h with LH (0.34 nM) in the presence or absence of tumor necrosis factor α (TNF; 2.9 nM) and interferon γ (IFNG; 2.5 nM) with or without P4 antagonist (onapristone, OP; 100 µM). Cell viability, and gene and protein expressions were measured by WST-1 assay, a real-time PCR and Western immunoblotting, respectively. [Results] LH reduced the levels of cell death induced by TNF and IFNG. LH attenuated mRNA expression of apoptosis related proteins, i.e. FAS, BAX and CASP3, as well as FAS and cleaved CASP3 protein expressions in TNF and IFNG treated cells. LH increased mRNA expression of BCL2 and BCL2:BAX mRNA ratio, whereas LH did not affect the BAX and BCL2 protein expression and BCL2:BAX protein ratio. Exposure to OP suppressed the anti-apoptotic effects of LH in the absence of TNF and IFNG. [Conclusion] The above results indicate that the anti-apoptotic effect of LH is mediated by increasing P4 production as well as by regulating the expression of apoptosis related proteins i.e. FAS, BAX, BCL2, CASP3 and cleaved CASP3. The overall results suggest that LH not only potentiates CL function but also protects LSC against apoptosis.
