TRPV1通过钙蛋白酶-蛋白酪氨酸磷酸酶途径减弱晶状体上皮细胞的上皮-间质转化。

IF 3 2区医学 Q1 OPHTHALMOLOGY

Experimental eye research Pub Date : 2025-05-24 DOI:10.1016/j.exer.2025.110435

Yosuke Nakazawa , Fuko Nishizawa , Sara Kawata , Yuki Sugiyama , Noriaki Nagai , Naoki Yamamoto , Megumi Funakoshi-Tago

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引用次数: 0

摘要

TRPV1是一种由辣椒素激活的非选择性阳离子通道，在全身广泛表达。我们之前报道过TRPV1激活通过抑制晶状体上皮细胞的表皮生长因子受体（EGFR）磷酸化抑制tgf - β2诱导的上皮-间质转化（EMT）（Sugiyama等，2021）。然而，具体的分子机制尚不清楚。在本研究中，我们重点研究了calpain-protein tyrosine phosphatase （PTP）通路，以阐明trpv1诱导EMT抑制的详细机制。在体外和离体实验中，Calpain和PTP抑制剂可减轻辣椒素对tgf - β2诱导的EMT的抑制作用。最后，我们发现CalpainS1和PTPN9过表达消除了辣椒素对晶状体上皮细胞EMT的影响。我们的研究结果表明calpain和PTP蛋白是预防白内障术后EMT的良好候选蛋白。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

TRPV1 attenuates epithelial-mesenchymal transition via calpain-protein tyrosine phosphatase pathway in lens epithelial cells

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TRPV1 attenuates epithelial-mesenchymal transition via calpain-protein tyrosine phosphatase pathway in lens epithelial cells

TRPV1, which is widely expressed throughout the body, is a non-selective cation channel activated by capsaicin. We previously reported that TRPV1 activation suppressed TGFβ2-induced epithelial-mesenchymal transition (EMT) by inhibiting Epidermal Growth Factor Receptor (EGFR) phosphorylation in lens epithelial cells (Sugiyama et al., 2021). However, the detailed molecular mechanism remains unclear. In this study, we focused on the calpain–protein tyrosine phosphatase (PTP) pathway to elucidate the detailed mechanism underlying TRPV1-induced EMT suppression. Calpain and PTP inhibitors mitigated the suppressive effect of capsaicin on TGFβ2-induced EMT in vitro and ex vivo. Finally, we shown that CalpainS1 and PTPN9 overexpression abrogated the effect of capsaicin on EMT in lens epithelial cells. Our findings indicate that calpain and PTP proteins are good candidates for preventing EMT after cataract surgery.

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来源期刊

Experimental eye research 医学-眼科学

CiteScore

6.80

自引率

5.90%

发文量

323

审稿时长

66 days

期刊介绍： The primary goal of Experimental Eye Research is to publish original research papers on all aspects of experimental biology of the eye and ocular tissues that seek to define the mechanisms of normal function and/or disease. Studies of ocular tissues that encompass the disciplines of cell biology, developmental biology, genetics, molecular biology, physiology, biochemistry, biophysics, immunology or microbiology are most welcomed. Manuscripts that are purely clinical or in a surgical area of ophthalmology are not appropriate for submission to Experimental Eye Research and if received will be returned without review.