miRNA-210 increased apoptosis of testicular tissues in cryptorchidism mice model through INHBB-Smad2/3 signaling pathway

Abstract

Background Cryptorchidism, as one of the common diseases of genitourinary abnormalities in newborn boys, has become an important factor leading to male infertility in the future. However, the specific pathogenesis remains poorly understood. The present experimental study aimed to clarify the mechanism of spermatogenic dysfunction caused by miR-210 in cryptorchidism. Methods In this study, 16 male ICR mice were classified into cryptorchidism group (n = 8), normal control group (n = 8), and the mice were killed in different age to create cryptorchidism self-control group. Then, the gene expression of miR-210 in testis tissues of three groups of mice, was detected by qPCR. HE staining and Tunel fluorescence staining were used to observe pathological changes and apoptosis of testis in cryptorchidism mice. The protein expression of INHBB was observed by immunohistochemistry. Finally, Western blot was used to detect the related proteins in the INHBB-Smad2/3-Casp3 pathway. Results The results indicated the expression of miR-210 was the most significant difference on the 14th day after cryptorchidism operation. We found that 14 days after the operation, apoptosis in the testis of cryptorchidism mice increased significantly. Finally, we found that the protein expressions of INHBB,Smad2/3, P-Smad2/3, and Caspase3 in the testicular tissues of cryptorchidism mice were significantly increased by detecting cryptorchidism mice with increased expression of miR-210. Conclusion Our results revealed the function of miR-210 and established the regulatory relationship between miR-210 and INHBB, which plays an important role in testicular tissue apoptosis.