Abstract
Follicular atresia is primarily induced by granulosa cell apoptosis; however, the molecular mechanisms that control apoptotic cell death in granulosa cells remain poorly understood. The present studies were undertaken to investigate the role of a novel endoplasmic reticulum stress-regulated gene Luman recruiting factor (LRF) in granulosa cell apoptosis during mouse follicular atresia. Based on immunohistochemistry and confocal laser scanning microscope analysis, LRF protein was localized in the cytoplasm of apoptotic granulosa cells, similar to localization of the LRF, Luman, CCAAT/enhancer-binding protein homologous protein and caspase-12 proteins were localized in apoptotic granulosa cells. However, glucose-regulated protein 78 protein was only present in healthy cells of the mural granulosa cell layers. A spontaneous onset of apoptotic cell death of granulosa cells was induced by thapsigargin or tunicamycin treatment in vitro, which was closely related to the increase of LRF, Luman, CCAAT/enhancer-binding protein homologous protein, and caspase-12 mRNA. Taken together, LRF might be involved in inducing apoptosis of granulosa cells through the endoplasmic reticulum stress pathway and might have a key role in mouse follicular selection.
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