Fig.Ā 9
From: Endothelium-specific deletion of p62 causes organ fibrosis and cardiac dysfunction
p62 interacts with FN1 and LAMC2 in endothelium cells, influencing their protein expression through the autophagy-lysosome pathway. A Quantitative real-time PCR (qRT-PCR) validation of FN1 and LAMC2 mRNA expression following p62 knockdown. B Immunoprecipitation (IP) assay confirming the interaction between p62 and FN1, as well as p62 and LAMC2. C Verification of FN1 and LAMC2 expression using the proteasome pathway inhibitor MG132 and the autophagy pathway inhibitor 3MA after p62 overexpression. D The autophagy inducer rapamycin exhibits potential in rescuing the accumulation of FN1 and LAMC2 caused by p62 knockdown. E Construction of truncated forms of p62 (PB1 and UBA), followed by IP to determine the binding regions of p62 with FN1 and LAMC2. F Mechanism diagram of tissue fibrosis caused by endothelial knockout in p62. ***pā<ā0.001