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ABSTRACT: Background
Nucleolin (NCL) plays an important regulatory role in angiotensin II (Ang II)-induced phenotypic switching of vascular smooth muscle cells (VSMCs). The aim of this study was to discuss its potential regulatory mechanisms.Results
We investigated if the pathways involving Ang II type 1 receptor (AT1R) and PKC/MAPK are responsible for Ang II's effects on VSMC phenotypic switching. Ang II upregulated NCL expression and activated the PKC/MAPK signaling pathway to induce VSMC phenotypic switching. In addition, Ang II promoted the translocation of NCL from the nucleus to the cell membrane. NCL was shown to bind to AT1R, whereas the binding of NCL to AT1R was greatly attenuated after the deletion of the GAR region. In addition, when peptide-N-glycosidase F (PNGase F) was
SUBMITTER: Fang L
PROVIDER: S-EPMC11863493 | biostudies-literature | 2025 Feb
REPOSITORIES: biostudies-literature