Estrogen-mediated TRPV5 modulates proliferation and apoptosis of rat cochlear hair cells via the PI3K/Akt pathway.

Abstract

OBJECTIVE: Transient Receptor Potential Vanilloid 5 (TRPV5) is an essential Catransporter mediated by estrogen in osteoclast differentiation and bone resorption. However, the mechanism of how estrogen mediates TRPV5 expression in Benign Paroxysmal Positional Vertigo (BPPV) remains unclear. METHODS: In this study, the Ovariectomized (OVX) rats were established to explore whether TRPV5 was regulated by estrogen. RESULTS: Lower protein expression level of TRPV5 showed in OVX rats were found to be restored by injection of Estradiol (E2). The same result was observed when TRPV5 expression was disturbed by si-TRPV5 fragment transfection. In addition, overexpression of TRPV5 up-regulated the expression of pho-Akt (Ser473) and promoted proliferation and apoptosis of cochlear hair cells. CONCLUSION: Estrogen may contribute to BPPV by stimulating TRPV5 overexpression to further up-regulate the expression of pho-Akt (Ser473) and promote cell proliferation and apoptosis. Our study provides preliminary insights into the pathogenesis of BPPV.