The Function And Regulatory Mechanism Of DDR2 Expression In Testis

Background:Disoind domain receptor 2(DDR2)is expressed in Leydig cell of normal human as well as mouse testis, and the DDR2slie/slie male mouse exhibits a phenotype of infertile. However, the function and regulatory of DDR2 expression in spermatogenesis remains unknown. Objective: To explore the infertile mechanism of DDR2slie/slie mouse as well as the function and regulatory mechanism of DDR2 expression in testis. Methods:We detected the DDR2 expression and function in spermatogenesis by establishing several infertilie mouse models and using testicular sections of infertile patient. Results:In our present study, we found DDR2 in Leydig cell could consume type I collagen in the interstitum while DDR2 deficiency caused deregulated expression of type I collagen may account for the disruption of the testicular steroidogenesis. We also revealed that the decrease of androgen receptor level in Sertoli cell of Sertoli cell only syndrome(SCOS) testis induced SC DDR2 expression and the SC DDR2 expression promoted SC phagocytosis and compemsated to repair blood-testis barrier. Furthermore, DDR2 expression in apoptotic germ cell of azoospermia testis and cryptorchidism testis was induced by tumor necrosis factor α(TNF-α) through nuclear factor κB(NF-κB) transcriptional regulation, the induced DDR2 inhibited germ cell apoptosis via suppressing FasL expression. Conclusion:In conclusion, we demonstrated DDR2 expression induced by different factors in different cell types played a vital role in maintaining spermatogenesis and repairing dyszoospermia.