ArticleJournal of molecular and cellular cardiology2021
YAP1/TEAD1 upregulate platelet-derived growth factor receptor beta to promote vascular smooth muscle cell proliferation and neointima formation.
Article in Journal of molecular and cellular cardiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Transcriptional control of PPP2CB by YAP1 and TEAD1 mediates AMPK inhibition and mTORC1 activation in vascular smooth muscle cells.iScience · 2026Article
- Smooth muscle cell phenotypic modulation during atherosclerosis.Vascular pharmacology · 2026Review
- EZH2 variants derived from cryptic splice sites govern distinct epigenetic patterns during embryonic development.Nucleic acids research · 2025Article
- Single-nuclei multiomics analysis identifies abnormal cardiomyocytes in a murine model of cardiac development.Nature communications · 2025Article
- Interplay between Skeletal Muscle Catabolism and Remodeling of Arteriovenous Fistula by Yes-Associated Protein 1 (YAP1) Signaling.Journal of the American Society of Nephrology : JASN · 2025Article
- Rosuvastatin activates autophagyThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Article
- O-GlcNAcylation-dependent liquid-liquid phase separation regulates the nuclear translocation of YAP to exacerbate vascular neointimal hyperplasia.Theranostics · 2025Article
- HIF-1α mediates hypertension and vascular remodeling in sleep apnea via hippo-YAP pathway activation.Molecular medicine (Cambridge, Mass.) · 2024Article
- Gut microbiota-derived Metabolite, Shikimic Acid, inhibits vascular smooth muscle cell proliferation and migration.Biochemical pharmacology · 2024Article
- PTPN14 aggravates neointimal hyperplasia via boosting PDGFRβ signaling in smooth muscle cells.Nature communications · 2024Article
- Spontaneous vascular dysfunction in Dahl salt-sensitive male rats raised without a high-salt diet.Physiological reports · 2024Article
- Hsa_circ_0031891 targets miR-579-3p to enhance HMGB1 expression and regulate PDGF-BB-induced human aortic vascular smooth muscle cell proliferation, migration, and dedifferentiation.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Receptor Tyrosine Kinase: Still an Interesting Target to Inhibit the Proliferation of Vascular Smooth Muscle Cells.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2023Review
- Article
- Six Decades of History of Hypertension Research at the University of Toledo: Highlighting Pioneering Contributions in Biochemistry, Genetics, and Host-Microbiota Interactions.Current hypertension reports · 2022Review
- Theaflavin-3,3'-Digallate from Black Tea Inhibits Neointima Formation Through Suppression of the PDGFRβ Pathway in Vascular Smooth Muscle Cells.Frontiers in pharmacology · 2022Article
- Infrapatellar Fat Pad-Synovial Membrane Anatomo-Fuctional Unit: Microscopic Basis for Piezo1/2 Mechanosensors Involvement in Osteoarthritis Pain.Frontiers in cell and developmental biology · 2022Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
We have previously demonstrated that the transcription co-factor yes-associated protein 1 (YAP1) promotes vascular smooth muscle cell (VSMC) de-differentiation. Yet, the role and underlying mechanisms of YAP1 in neointima formation in vivo remain unclear. The goal of this study was to investigate the role of VSMC-expressed YAP1 in vascular injury-induced VSMC proliferation and delineate the mechanisms underlying its action. Experiments employing gain- or loss-of-function of YAP1 demonstrated that YAP1 promotes human VSMC proliferation. Mechanistically, we identified platelet-derived growth factor receptor beta (PDGFRB) as a novel YAP1 target gene that confers the YAP1-dependent hyper-proliferative effects in VSMCs. Furthermore, we identified TEA domain transcription factor 1 (TEAD1) as a key transcription factor that mediates YAP1-dependent PDGFRβ expression. ChIP assays demonstrated that TEAD1 is enriched at a PDGFRB gene enhancer. Luciferase reporter assays further demonstrated that YAP1 and TEAD1 co-operatively activate the PDGFRB enhancer. Consistent with these observations, we found that YAP1 expression is upregulated after arterial injury and correlates with PDGFRβ expression and VSMC proliferation in vivo. Using a novel inducible SM-specific Yap1 knockout mouse model, we found that the specific deletion of Yap1 in adult VSMCs is sufficient to attenuate arterial injury-induced neointima formation, largely due to inhibited PDGFRβ expression and VSMC proliferation. Our study unravels a novel mechanism by which YAP1/TEAD1 promote VSMC proliferation via transcriptional induction of PDGFRβ, thereby enhancing PDGF-BB downstream signaling and promoting neointima formation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.