Heat Stress Induces Autophagy in Pig Ovaries during Follicular Development

Hyperthermia or heat stress (HS) compromises swine reproduction through many mechanisms and occurs when body temperature rises above a level no longer controllable by panting and evaporative cooling. Autophagy is a process by which somatic cells recycle energy through the reutilization of cellular components and is activated by a variety of stressors. The objective of this study was to characterize autophagy-related protein abundance and localization in the ovary following cyclical HS experienced during the follicular phase preceding ovulation. To accomplish this, twelve gilts were synchronized using an altrenogest (a progesterone receptor agonist) administered orally for 14 days and subjected for cyclical HS (n = 6) or thermal neutral (TN; n = 6) conditions for 5 days following altrenogest withdrawal during the follicular phase. Ovarian protein abundance of BECN1 and LC3B-II were each elevated approximately 5-fold as a result of HS (P = 0.001 and 0.003, respectively). Regulation of autophagy and apoptosis occurs in tight coordination, and BCL-XL can regulate both processes. BCL-XL abundance, as detected via immunofluorescence, was increased in both oocytes (~1.6-fold; P < 0.01) and granulosa cells of primary follicles (~1.4-fold P < 0.05) in HS compared to TN ovaries, suggesting inhibition of apoptosis. These results suggest that induction of autophagy occurs in the ovary in response to HS during the follicular phase, and that HS increases anti-apoptotic signaling in oocytes and early follicles. Understanding how HS affects the ovary is critical to mitigate heat stress-mediated compromise of reproductive ability in domestic livestock species.