Polypyrimidine tract-binding protein 1 regulates the Sertoli cell blood-testis barrier by promoting the expression of tight junction proteins

xlomafota13 shared this article with you from Inoreader Polypyrimidine tract-binding protein 1 regulates the Sertoli cell blood-testis barrier by promoting the expression of tight junction proteins Via Experimental and therapeutic medicine Exp Ther Med. 2021 Aug;22(2):847. doi: 10.3892/etm.2021.10279. Epub 2021 Jun 7. ABSTRACT Sertoli cells (SCs) are an important component of spermatogenic tubules. The blood-testis barrier (BTB) is composed of SCs and is necessary for the development and maturity of spermatogenic cells. When the tight connection between SCs is destroyed, the BTB loses its integrity, leading to impaired spermatogenesis. Polypyrimidine tract-binding protein 1 (PTBP1) is a key protein involved in precursor mRNA splicing and selective splicing events, which directly affects tumor cell proliferation and influences the formation of the blood-tumor barrier by regulating the expression levels of tight junction-associated proteins. The present study revealed that the expression of PTBP1 was downregulated following a decrease in spermatogenic activity at the phase of senescence. TM4 cells were transfected with lentivirus-short hairpinRNA-PTBP1 to evaluate the effe ct of silencing PTBP1 on the expression levels of tight junction proteins and the integrity of tight junctions between adjacent SCs. Western blot analysis indicated that the expression levels of Zonula occludens 1, occludin and claudin-5 decreased significantly due to silencing of PTBP1 in SCs. Through detecting trans-epithelial electrical resistance, it was revealed that silencing of PTBP1 broke the integrity of tight junctions between adjacent SCs. The results suggested that PTBP1 maintained the integrity of the BTB by promoting the expression levels of tight junction-associated proteins and revealed the possible mechanism of PTBP1 in regulating spermatogenesis. PMID:34149893 | PMC:PMC8210256 | DOI:10.3892/etm.2021.10279 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.