Endothelium-specific deletion of p62 causes organ fibrosis and cardiac dysfunction.

ABSTRACT:

Background

The autophagy adapter SQSTM1/p62 is crucial for maintaining homeostasis in various organs and cells due to its protein-protein interaction domains and involvement in diverse physiological and pathological processes. Vascular endothelium cells play a unique role in vascular biology and contribute to vascular health.

Methods

Using the Cre-loxP system, we generated mice with endothelium cell-specific knockout of p62 mediated by Tek (Tek receptor tyrosine kinase)-cre to investigate the essential role of p62 in the endothelium. In vitro, we employed protein mass spectrometry and IPA to identify differentially expressed proteins upon knockdown of p62. Immunoprecipitation assays were conducted to demonstrate the interaction between p62 and FN1 or LAMC2 in human umbilical

SUBMITTER: Feng J 

PROVIDER: S-EPMC10870664 | biostudies-literature | 2024 Feb

REPOSITORIES: biostudies-literature