Endoplasmic Reticulum Stress Is Involved in Prostaglandin F2 <i>α</i> ‐Induced Goat Luteal Cell Apoptosis via the <scp>IRE1</scp> Pathway

In mammals, the corpus luteum (CL) is an endocrine gland whose function and survival are limited in scope and time. Although the CL produces progesterone to maintain pregnancy, regression of the CL is necessary for initiating the estrous cycle. A previous study showed that prostaglandin F2α (PGF2α) is a luteolysis hormone that causes CL regression by inducing luteal cell apoptosis. Although much is known about the role of PGF2α during luteolysis, the functions of endoplasmic reticulum (ER) stress and the unfolded protein response (UPR) in PGF2α-induced CL regression are unclear. In this study, goat luteal cells were treated with PGF2α to trigger apoptosis. We found that ER stress was induced by PGF2α treatment. Additionally, the ER stress-mediated UPR was activated through its three sensors (IRE1, ATF6 and PERK) in goat luteal cells. By applying different ER stresses, we revealed the role of ER stress in PGF2α-induced apoptosis in goat luteal cells. Further, IRE1 knockdown inhibited mitochondrial pathway-mediated apoptosis in luteal cells. Together, our results indicate that the ER stress-mediated UPR promotes goat luteal cell apoptosis, which is related to IRE1 activation in mitochondrial pathway-mediated apoptosis. This present work may provide new insight into the mechanistic pathways of regulating regression of goat CL.