Estradiol Alleviates Elevated Temperature-Induced Damage in Yak Oviductal Epithelial Cells by Maintaining Endoplasmic Reticulum Calcium Homeostasis.

Abstract

Background: The oviduct is an organ that participates in multiple critical reproductive processes and provides essential nutritional support while maintaining a specialized microenvironment. It is particularly vulnerable to damage following heat stress-induced hyperthermia. Therefore, mitigating heat-induced damage to oviduct epithelial cells while preserving their physiological integrity under hyperthermia represents a critical therapeutic goal.

Objective: This study aims to simulate the cellular damage state in yak oviduct epithelial cells (YOECs) under thermal challenge by increasing the incubation temperature of cultured cells, while observing changes in cellular injury upon supplementation with 17β-estradiol (E₂), in order to explore the underlying cellular regulatory mechanisms involved.

Results: After 48 h of exposure to 41 °C, YOECs exhibited elevated HSP70 and HSP90 protein expression levels, reduced OVGP1 protein expression, and increased apoptotic cells. Compared to the 41 °C group, the E₂ + 41 °C group displayed decreased HSP70 protein levels, increased OVGP1 protein expression, and reduced apoptotic cell numbers. Additionally, changes in endoplasmic reticulum calcium ion (ER-Ca²⁺) distribution and fluorescence intensity variations in ER-Ca²⁺ regulatory proteins SERCA and IP3R3 were analyzed in the 37 °C, 41 °C, and E₂ + 41 °C groups. The ER-Ca²⁺ distribution pattern in the E₂ + 41 °C group remained similar to that of the 37 °C group. However, the fluorescence intensity levels of SERCA and IP3R3 proteins in the E₂ + 41 °C group did not recover to levels comparable to the 37 °C group.

Conclusion: These findings suggest that E₂ may mitigate thermal challenge-induced cellular damage in YOECs by maintaining ER-Ca²⁺ homeostasis, thereby preserving cellular functionality under elevated temperatures.