Scholarlink

Objective <p>Microcystin-LR (MC-LR) targets Sertoli cells (SCs), induces reproductive toxicity, disrupts the immune-privileged microenvironment of the blood–testis barrier (BTB), and consequently impairs spermatogenesis. However, whether the bitter taste receptor <i>mT2R143</i> is involved in the mechanisms by which SCs resist toxicant uptake and preserve immune homeostasis following MC-LR exposure remains unclear.</p> Methods <p>In this study, TM4 cells were exposed to different concentrations of MC-LR (1&#xa0;μM, 0.5&#xa0;μM, and 0.05&#xa0;μM) for 24&#xa0;h and 48&#xa0;h, and the expression of related molecular markers was examined using qPCR, Western blot, and immunofluorescence.</p> Results <p>MC-LR exposure significantly upregulated <i>mT2R143</i> mRNA expression (<i>P</i> &lt; 0.05). Co-treatment with MC-LR and siRNA-<i>mT2R143</i> markedly downregulated the expression of the BTB tight junction proteins ZO-1 and Occludin compared with the control group (<i>P</i> &lt; 0.01). Immunofluorescence analysis further confirmed the reduction of ZO-1 and Occludin. Similarly, combined exposure to MC-LR and an NF-κB inhibitor led to a significant decrease in ZO-1 and Occludin (<i>P</i> &lt; 0.01).</p> Conclusion <p>These findings suggest that MC-LR exposure activates <i>mT2R143</i> expression in TM4 cells and that <i>mT2R143</i> mediates NF-κB signaling to regulate the expression of BTB tight junction proteins. This work provides a theoretical basis for exploring the regulatory roles of bitter taste receptors in the reproductive system, highlights their potential involvement in the chemosensory regulation of spermatogenesis, and offers new perspectives for testicular reproductive toxicology research.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

mT2R143/NF-κB signaling pathway regulates the expression of the blood–testis barrier tight junction protein in TM4 exposed to microcystin-LR

  • 期刊论文

  • 发表日期：

    2026年5月27日

查看全文
  • Xiaodong Hu,
  • Jindan Wang,
  • Jiaqi Yao,
  • Ruxue Deng,
  • Lei Xia,
  • Xue Wang

摘要

Objective

Microcystin-LR (MC-LR) targets Sertoli cells (SCs), induces reproductive toxicity, disrupts the immune-privileged microenvironment of the blood–testis barrier (BTB), and consequently impairs spermatogenesis. However, whether the bitter taste receptor mT2R143 is involved in the mechanisms by which SCs resist toxicant uptake and preserve immune homeostasis following MC-LR exposure remains unclear.

Methods

In this study, TM4 cells were exposed to different concentrations of MC-LR (1 μM, 0.5 μM, and 0.05 μM) for 24 h and 48 h, and the expression of related molecular markers was examined using qPCR, Western blot, and immunofluorescence.

Results

MC-LR exposure significantly upregulated mT2R143 mRNA expression (P < 0.05). Co-treatment with MC-LR and siRNA-mT2R143 markedly downregulated the expression of the BTB tight junction proteins ZO-1 and Occludin compared with the control group (P < 0.01). Immunofluorescence analysis further confirmed the reduction of ZO-1 and Occludin. Similarly, combined exposure to MC-LR and an NF-κB inhibitor led to a significant decrease in ZO-1 and Occludin (P < 0.01).

Conclusion

These findings suggest that MC-LR exposure activates mT2R143 expression in TM4 cells and that mT2R143 mediates NF-κB signaling to regulate the expression of BTB tight junction proteins. This work provides a theoretical basis for exploring the regulatory roles of bitter taste receptors in the reproductive system, highlights their potential involvement in the chemosensory regulation of spermatogenesis, and offers new perspectives for testicular reproductive toxicology research.