ArticleBiology direct2025
Nucleolin in the cell membrane promotes Ang II-mediated VSMC phenotypic switching by regulating the AT1R internalization function : Nucleolin promotes Ang II-mediated VSMC phenotypic switching.
Article in Biology direct, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- The role of caveolin-1 in atherosclerosis and its molecular mechanism.Lipids in health and disease · 2026Review
- Therapeutic Implication of Anti-CTGF in Neointimal Hyperplasia via Regulating Mitochondrial Dysfunction and VSMC Phenotypic Switch.Cardiovascular therapeutics · 2026Article
- A catalase nanocapsule inhibits VSMCs proliferation and migration through PTEN/NLRP3 pathway.Frontiers in pharmacology · 2026Article
- Role of vascular smooth muscle phenotypic transformation induced by histone modifications in the development of abdominal aortic aneurysms.Clinical epigenetics · 2025Review
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Authors and funding
6 authors.
Funding
Abstract
backgroundNucleolin (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.
resultsWe 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 applied, the N-glycosylation of NCL protein and the phenotypic switching of VSMC were inhibited. Ang II-induced AT1R internalization, whereas overexpression of NCL delayed Ang II-induced AT1R internalization by inhibiting AT1R phosphorylation and recruited Rab4 and Rab11 to promote recycling, and knockdown of NCL showed the opposite effect and reversal of AT1R binding by the use of rasarfin reversed the effects of sh-NCL. In in vivo experiments, knockdown of NCL expression inhibited Ang II-induced blood pressure rise and vasculopathy.
conclusionsOur study demonstrates that NCL promotes Ang II-mediated phenotypic switching of VSMCs by regulating AT1R internalization function.
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