Effect of Heat Stress on Egg Production, Steroid Hormone Synthesis, and Related Gene Expression in Chicken Preovulatory Follicular Granulosa Cells

Simple Summary The debilitating effects of heat stress on poultry production have been well documented. Heat stress already results in severe economic loss worldwide. Regarding the decline in the reproductive performance of heat-stressed hens, the exact mechanisms involved are still unknown. The present study was conducted to elucidate the molecular mechanisms underlying heat-stress-induced abnormal egg production in laying hens. Our results confirmed that laying hens reared under heat stress had impaired laying performance. Follicular granulosa cells cultured in vitro are sensitive to the effects of heat stress, showing an increase in apoptosis and cellular ultrastructural changes. These effects appeared in the form of heat-stress-elevated progesterone, with the increased expression of steroidogenic acute regulatory protein, cytochrome P450 family 11 subfamily A member 1, and 3b-hydroxysteroid dehydrogenase, along with inhibited estradiol synthesis through the decreased expression of follicle-stimulating hormone receptor and the cytochrome P450 family 19 subfamily A member 1. Collectively, laying hens exposed to high temperatures showed damage to granulosa cells that brought about a decline in egg production. This study provides a molecular mechanism for the abnormal laying performance of hens subjected to heat stress, which may help when developing novel strategies to reverse the adverse impact. This study was conducted to elucidate the molecular mechanisms underlying heat stress (HS)-induced abnormal egg-laying in laying hens. Hy-Line brown laying hens were exposed to HS at 32 degrees C or maintained at 22 degrees C (control) for 14 days. In addition, granulosa cells (GCs) from preovulatory follicles were subjected to normal (37 degrees C) or high (41 degrees C or 43 degrees C) temperatures in vitro. Proliferation, apoptosis, and steroidogenesis were investigated, and the expression of estrogen and progesterone synthesis-related genes was detected. The results confirmed that laying hens reared under HS had impaired laying performance. HS inhibited proliferation, increased apoptosis, and altered the GC ultrastructure. HS also elevated progesterone secretion by increasing the expression of steroidogenic acute regulatory protein (StAR), cytochrome P450 family 11 subfamily A member 1 (CYP11A1), and 3b-hydroxysteroid dehydrogenase (3 beta-HSD). In addition, HS inhibited estrogen synthesis in GCs by decreasing the expression of the follicle-stimulating hormone receptor (FSHR) and cytochrome P450 family 19 subfamily A member 1 (CYP19A1). The upregulation of heat shock 70 kDa protein (HSP70) under HS was also observed. Collectively, laying hens exposed to high temperatures experienced damage to follicular GCs and steroidogenesis dysfunction, which reduced their laying performance. This study provides a molecular mechanism for the abnormal laying performance of hens subjected to HS.