Inflammatory Signaling via PEIZO1 Engages and Enhances the LPS-Mediated Apoptosis during Clinical Mastitis,Journal of Agricultural and Food Chemistry

当前位置： X-MOL 学术 › J. Agric. Food Chem. › 论文详情

Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)

Inflammatory Signaling via PEIZO1 Engages and Enhances the LPS-Mediated Apoptosis during Clinical Mastitis
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2024-09-04 , DOI: 10.1021/acs.jafc.4c04421
Jingyi Wang ₁ , Ming Li ₁ , Wenda Wu ₂ , HuiJing Zhang ₁ , Yue Yang ₁ , Muhammad Usman ₃ , Ben Aernouts ₄ , Juan J Loor ₃ , Chuang Xu ₁

Affiliation

Bovine clinical mastitis is characterized by inflammation and immune responses, with apoptosis of mammary epithelial cells as a cellular reaction to infection. PIEZO1, identified as a mechanotransduction effector channel in nonruminant animals and sensitive to both mechanical stimuli or inflammatory signals like lipopolysaccharide (LPS). However, its role in inflammatory processes in cattle has not been well-documented. The aim of this study was to elucidate the in situ expression of PIEZO1 in bovine mammary gland and its potential involvement in clinical mastitis. We observed widespread distribution and upregulation of PIEZO1 in mammary epithelial cells in clinical mastitis cows and LPS-induced mouse models, indicating a conserved role across species. In vitro studies using mammary epithelial cells (MAC-T) revealed that LPS upregulates PIEZO1. Notably, the effects of PIEZO1 artificial activator Yoda1 increased apoptosis and NLRP3 expression, effects mitigated by PIEZO1 silencing or NLRP3 inhibition. In conclusion, the activation of the PIEZO1-NLRP3 pathway induces abnormal apoptosis in mammary epithelial cells, potentially serving as a regulatory mechanism to combat inflammatory responses to abnormal stimuli.

中文翻译：

通过 PEIZO1 的炎症信号传导并增强临床乳腺炎期间 LPS 介导的细胞凋亡

牛临床乳腺炎的特征是炎症和免疫反应，乳腺上皮细胞凋亡是对感染的细胞反应。 PIEZO1，被确定为非反刍动物中的机械转导效应通道，对机械刺激或脂多糖 (LPS) 等炎症信号敏感。然而，它在牛炎症过程中的作用尚未得到充分记录。本研究的目的是阐明PIEZO1在牛乳腺中的原位表达及其在临床乳腺炎中的潜在参与。我们观察到 PIEZO1 在临床乳腺炎奶牛和 LPS 诱导的小鼠模型的乳腺上皮细胞中广泛分布和上调，表明跨物种的保守作用。使用乳腺上皮细胞 (MAC-T) 的体外研究表明，LPS 上调 PIEZO1。值得注意的是，PIEZO1 人工激活剂 Yoda1 的作用增加了细胞凋亡和 NLRP3 的表达，而 PIEZO1 沉默或 NLRP3 抑制可以减轻这种影响。总之，PIEZO1-NLRP3 通路的激活会诱导乳腺上皮细胞异常凋亡，可能作为对抗异常刺激引起的炎症反应的调节机制。

更新日期：2024-09-04

点击分享查看原文

点击收藏

阅读更多本刊新发论文本刊介绍/投稿指南