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Piezo1可选择性增强B细胞由转化生长因子-β1诱导的IgA类别转换。

Piezo1 selectively enhances TGF-β1-induced IgA class switching by B cells.

作者信息

Jung Yoonji, Han Younghwan, Kang Jaeku, Yu Seong-Lan, Park Seok-Rae

机构信息

Department of Microbiology, Konyang University College of Medicine, 158 Gwanjeodong-ro, Seo-gu, Daejeon, 35365, Korea.

Priority Research Center, Myunggok Medical Research Institute, Konyang University College of Medicine, Daejeon, 35365, Korea.

出版信息

Cell Mol Life Sci. 2025 Jun 19;82(1):243. doi: 10.1007/s00018-025-05789-4.

Abstract

Piezo1 is a mechanosensitive cationic channel that regulates Ca influx, gene transcription, and cell migration. Recent studies suggest that Piezo1 affects regulatory T cells differentiation and is critical in B cell responses to membrane-presented antigens. However, the role of Piezo1 in B cells function is not completely elucidated. This study investigated the role of Piezo1 in IgA class switching and Ab production by mouse B cells using qRT-PCR, flow cytometric analysis, and isotype-specific ELISA. The Piezo1 agonist Yoda1 selectively upregulated TGF-β1-induced germline α transcripts (GLTα) /post-switch α transcripts (GLTα) expression, surface IgA expression, and IgA production. Conversely, the Piezo1 inhibitor OB-1 reduced IgA class switching. TGF-β1-induced IgA class switching and IgA production decreased in Piezo1 knockdown B cells. Additionally, Piezo1 enhanced TGF-β1-induced Smad3 phosphorylation. These results demonstrate that Piezo1 selectively enhances TGF-β1-induced IgA class switching via Smad3 phosphorylation, leading to IgA production in B cells.

摘要

Piezo1是一种机械敏感阳离子通道,可调节钙离子内流、基因转录和细胞迁移。最近的研究表明,Piezo1影响调节性T细胞的分化,并且在B细胞对膜呈现抗原的反应中起关键作用。然而,Piezo1在B细胞功能中的作用尚未完全阐明。本研究使用qRT-PCR、流式细胞术分析和同型特异性ELISA,研究了Piezo1在小鼠B细胞IgA类别转换和抗体产生中的作用。Piezo1激动剂Yoda1选择性地上调了转化生长因子-β1(TGF-β1)诱导的种系α转录本(GLTα)/转换后α转录本(PSα)的表达、表面IgA的表达以及IgA的产生。相反,Piezo1抑制剂OB-1减少了IgA类别转换。在Piezo1敲低的B细胞中,TGF-β1诱导的IgA类别转换和IgA产生减少。此外,Piezo1增强了TGF-β1诱导的Smad3磷酸化。这些结果表明,Piezo1通过Smad3磷酸化选择性地增强TGF-β1诱导的IgA类别转换,从而导致B细胞中IgA的产生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81cf/12179034/4da9a083d847/18_2025_5789_Fig1_HTML.jpg

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