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Tas2R143 regulates the expression of the Blood-Testis Barrier tight junction protein in TM4 cells through the NF-κB signaling pathway.

Authors :
Wang X
Wang JD
Li X
Wang T
Yao J
Deng R
Ma W
Liu S
Zhu Z
Source :
Theriogenology [Theriogenology] 2024 Oct 01; Vol. 227, pp. 120-127. Date of Electronic Publication: 2024 Jul 10.
Publication Year :
2024

Abstract

Although bitter receptors, known as Tas2Rs, have been identified in the testes and mature sperm, their expression in testicular Sertoli cells (SCs) and their role in recognizing harmful substances to maintain the immune microenvironment remain unknown. To explore their potential function in spermatogenesis, this study utilized TM4 cells and discovered the high expression of the bitter receptor Tas2R143 in the cells. Interestingly, when the Tas2R143 gene was knocked down for 24 and 48 h, there was a significant downregulation (P < 0.05) in the expression of tight junction proteins (occludin and ZO-1) and NF-κB. Additionally, Western blot results demonstrated that the siRNA-133+NF-κB co-treatment group displayed a significant downregulation (P < 0.05) in the expression of occludin and ZO-1 compared to both the siRNA-133 transfection group and the NF-κB inhibitors treatment group. These findings suggest that Tas2R143 likely regulates the expression of occludin and ZO-1 through the NF-κB signaling pathway and provides a theoretical basis for studying the regulatory mechanism of bitter receptors in the reproductive system, aiming to attract attention to the chemical perception mechanism of spermatogenesis.<br />Competing Interests: Declaration of competing interest The authors declare that the research was conducted without any commercial or financial relationships that could be construed as a potential conflict of interest.<br /> (Copyright © 2024. Published by Elsevier Inc.)

Details

Language :
English
ISSN :
1879-3231
Volume :
227
Database :
MEDLINE
Journal :
Theriogenology
Publication Type :
Academic Journal
Accession number :
39059123
Full Text :
https://doi.org/10.1016/j.theriogenology.2024.07.005