Lipopolysaccharide-induced podocyte injury is regulated by calcineurin/NFAT and TLR4/MyD88/NF-κB signaling pathways through angiopoietin-like protein 4

Xiujin Shen; Chunhua Weng; Yucheng Wang; Cuili Wang; Shi Feng; Xiayu Li; Heng Li; Hong Jiang; Haibing Wang; Jianghua Chen

doi:10.1016/j.gendis.2020.07.005

您当前的位置：

首页 >

文章列表页 >

Lipopolysaccharide-induced podocyte injury is regulated by calcineurin/NFAT and TLR4/MyD88/NF-κB signaling pathways through angiopoietin-like protein 4

Full-length article | 更新时间：2022-06-24

- Lipopolysaccharide-induced podocyte injury is regulated by calcineurin/NFAT and TLR4/MyD88/NF-κB signaling pathways through angiopoietin-like protein 4
- Lipopolysaccharide-induced podocyte injury is regulated by calcineurin/NFAT and TLR4/MyD88/NF-κB signaling pathways through angiopoietin-like protein 4
- Genes & Diseases 2022年9卷第2期
- 作者机构：
  
  1. Kidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University,Hangzhou,PR China,310003
  2. Key Laboratory of Kidney Disease Prevention and Control Technology,Zhejiang Province,Hangzhou,PR China,310063
  3. National Key Clinical Department of Kidney Diseases,Hangzhou,PR China,310005
  4. Institute of Nephrology, Zhejiang University,Hangzhou,PR China,310020
  5. The Third Grade Laboratory under the National State, Administration of Traditional Chinese Medicine,Hangzhou,PR China,310005
  6. Central Laboratory, the First Affiliated Hospital of Zhejiang Chinese Medical University,Hangzhou,PR China,310006
- 作者简介：
- 基金信息：
- DOI：10.1016/j.gendis.2020.07.005
  中图分类号：
- 纸质出版日期：2022，
  
  网络出版日期：2022-3-1，
扫描看全文
Xiujin Shen, Chunhua Weng, Yucheng Wang, 等. Lipopolysaccharide-induced podocyte injury is regulated by calcineurin/NFAT and TLR4/MyD88/NF-κB signaling pathways through angiopoietin-like protein 4[J]. Genes & Diseases, 2022,9(2).

Xiujin Shen, Chunhua Weng, Yucheng Wang, et al. Lipopolysaccharide-induced podocyte injury is regulated by calcineurin/NFAT and TLR4/MyD88/NF-κB signaling pathways through angiopoietin-like protein 4[J]. Genes & Diseases, 2022,9(2).
Xiujin Shen, Chunhua Weng, Yucheng Wang, 等. Lipopolysaccharide-induced podocyte injury is regulated by calcineurin/NFAT and TLR4/MyD88/NF-κB signaling pathways through angiopoietin-like protein 4[J]. Genes & Diseases, 2022,9(2). DOI： 10.1016/j.gendis.2020.07.005.

Xiujin Shen, Chunhua Weng, Yucheng Wang, et al. Lipopolysaccharide-induced podocyte injury is regulated by calcineurin/NFAT and TLR4/MyD88/NF-κB signaling pathways through angiopoietin-like protein 4[J]. Genes & Diseases, 2022,9(2). DOI： 10.1016/j.gendis.2020.07.005.

摘要

Abstract

Podocyte injury is an important cause of proteinuria. Angiopoietin-like protein 4 (Angptl4) is a secreted glycoprotein and has a role in proteinuria. However

the exact role of Angptl4 in podocyte injury and its upstream regulators has not been clarified. In this study

we used lipopolysaccharide (LPS)-induced mice and cultured podocytes as podocyte injury models. Our results indicated that LPS increased the expression of podocyte Angptl4

in vivo

and

in vitro

. Furthermore

we showed that Angptl4 overexpression deteriorated LPS-induced podocyte injury by inducing podocyte cytoskeleton rearrangement

reducing the expression of synaptopodin while Angptl4 knockdown alleviated LPS-induced podocyte injury. In addition

we found that inhibitors and siRNA targeting TLR4/MyD88/NF-κB signaling inhibited the upregulation of Angptl4 in LPS-induced podocytes. Moreover

inhibitors and siRNA targeting calcineurin/NFAT signaling also relieved LPS-induced Angptl4 expression and podocyte injury

in vivo

and

in vitro

. Taken together

our study has elucidated that both of the TLR4/MyD88/NF-κB and calcineurin/NFAT signaling mediate the upregulation of Angptl4 in LPS-induced podocytes

which has important implications for further understanding the molecular mechanism of LPS-induced podocyte injury.

关键词

Keywords

Angiopoietin-like protein 4Calcineurin/NFATLPSPodocyte injuryTLR4/MyD88/NF-κB

references

查看原文

浏览量

下载量

CSCD

文章被引用时，请邮件提醒。

提交

工具集

关联资源

暂无数据