ArticleMolecular and cellular biochemistry2018
CD137-CD137L interaction modulates neointima formation and the phenotype transformation of vascular smooth muscle cells via NFATc1 signaling.
Article in Molecular and cellular biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- TNF superfamily molecules in atherosclerosis: mechanistic insights and therapeutic translation.Frontiers in immunology · 2025Review
- The Exacerbating Effects of the Tumor Necrosis Factor in Cardiovascular Stenosis: Intimal Hyperplasia.Cancers · 2024Review
- Dynamic phenotypic shifts and M2 receptor downregulation in bladder smooth muscle cells induced by mirabegron.Frontiers in pharmacology · 2024Article
- Calcineurin Is a Universal Regulator of Vessel Function-Focus on Vascular Smooth Muscle Cells.Cells · 2023Review
- How vascular smooth muscle cell phenotype switching contributes to vascular disease.Cell communication and signaling : CCS · 2022Review
- Article
- Role of NFAT in the Progression of Diabetic Atherosclerosis.Frontiers in cardiovascular medicine · 2021Review
- MicroRNA-342-5p activates the Akt signaling pathway by downregulating PIK3R1 to modify the proliferation and differentiation of vascular smooth muscle cells.Experimental and therapeutic medicine · 2020Article
- Paving the Way toward Successful Multiple Myeloma Treatment: Chimeric Antigen Receptor T-Cell Therapy.Cells · 2020Review
- CD137 Signaling Promotes Endothelial Apoptosis by Inhibiting Nrf2 Pathway, and Upregulating NF-Mediators of inflammation · 2020Article
- Hypoxia-Induced Phenotypic Transformation of Corpus Cavernosum Smooth Muscle Cells After Cavernous Nerve Crush Injury by Down-Regulating P38 Mitogen-Activated Protein Kinase Expression.Sexual medicine · 2019Article
- Recent updates on CAR T clinical trials for multiple myeloma.Molecular cancer · 2019Review
- Hypermethylation of the Micro-RNA 145 Promoter Is the Key Regulator for NLRP3 Inflammasome-Induced Activation and Plaque Formation.JACC. Basic to translational science · 2018Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular smooth muscle cell (VSMC) phenotype transformation is an important event in the formation of vessel neointima during lesion progression. CD137 can accelerate plaque formation, but the underlying mechanisms of this process remain unknown. Thus, we investigated the effect of CD137 signaling on VSMC phenotype transformation and potential mechanism underlying this transformation. Mouse recombinant CD137L and anti-CD137 antibody were used to activate or block the CD137 signaling way, respectively. Real-time PCR, immunofluorescence, and western blot analyses were performed to detect the expression of NFATc1 and phenotype markers such as SM-MHC, α-SMA, and vimentin in vivo or in vitro. Inhibition of NFATc1 expression was established by small interfering RNA (siRNA) and lentivirus in vitro and in vivo, respectively. Plenti-virus vector was constructed to overexpress NFATc1. Transwell assay was used to detect the migration ability of cells. The expression of NFATc1 was significantly upregulated by treating VSMCs with CD137L. The contractile phenotype markers decreased, while the synthesis phenotype marker and cell migration increased after CD137 stimulation. This phenomenon can be blocked by combined use of anti-CD137 antibody or siRNA of NFATc1. Overexpression of NFATc1 caused the VSMC phenotype transformation independently. In conclusion, the CD137-CD137L pathway plays an important role in regulating VSMC phenotype transformation via activation of NFATc1 signaling pathway.
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