ArticleEBioMedicine2019
Semaphorin-3A protects against neointimal hyperplasia after vascular injury.
Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Progress in research on the role of exosomal miRNAs in the diagnosis and treatment of cardiovascular diseases.Frontiers in genetics · 2022Pooled it
- Selective vulnerability of cerebral vasculature toScience advances · 2026Article
- Semaphorin 3A protects against thoracic aortic aneurysm dissection by suppressing aortic angiogenesis.Angiogenesis · 2025Article
- Neuroimmune circuits in the plaque and bone marrow regulate atherosclerosis.Cardiovascular research · 2025Review
- TTK Inhibition Alleviates Postinjury Neointimal Formation and Atherosclerosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- SOX9 mediates the phenotypic transformation of vascular smooth muscle cells in restenosis after carotid artery injury.Frontiers in cell and developmental biology · 2025Article
- Reduced expression of semaphorin 3A in osteoclasts causes lymphatic expansion in a Gorham-Stout disease (GSD) mouse model.Journal of Zhejiang University. Science. B · 2024Article
- miRNA‑92a inhibits vascular smooth muscle cell phenotypic modulation and may help prevent in‑stent restenosis.Molecular medicine reports · 2023Article
- Role of Semaphorins in Ischemic Stroke.Frontiers in molecular neuroscience · 2022Review
- Sterol-resistant SCAP Overexpression in Vascular Smooth Muscle Cells Accelerates Atherosclerosis by Increasing Local Vascular Inflammation through Activation of the NLRP3 Inflammasome in Mice.Aging and disease · 2021Article
- The P2RY12 receptor promotes VSMC-derived foam cell formation by inhibiting autophagy in advanced atherosclerosis.Autophagy · 2021Article
- Neuronal guidance proteins in cardiovascular inflammation.Basic research in cardiology · 2021Review
- A Novel Resveratrol Analog Upregulates SIRT1 Expression and Ameliorates Neointima Formation.Frontiers in cardiovascular medicine · 2021Article
- The Entry and Egress of Monocytes in Atherosclerosis: A Biochemical and Biomechanical Driven Process.Cardiovascular therapeutics · 2021Review
- JANEX-1 improves acute pulmonary embolism through VEGF and FAK in pulmonary artery smooth muscle cells.Experimental biology and medicine (Maywood, N.J.) · 2020Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeointimal hyperplasia is a prominent pathological event during in-stent restenosis. Phenotype switching of vascular smooth muscle cells (VSMCs) from a differentiated/contractile to a dedifferentiated/synthetic phenotype, accompanied by migration and proliferation of VSMCs play an important role in neointimal hyperplasia. However, the molecular mechanisms underlying phenotype switching of VSMCs have yet to be fully understood.
methodsThe mouse carotid artery ligation model was established to evaluate Sema3A expression and its role during neointimal hyperplasia in vivo. Bioinformatics analysis, chromatin immunoprecipitation (ChIP) assays and promoter-luciferase reporter assays were used to examine regulatory mechanism of Sema3A expression. SiRNA transfection and lentivirus infection were performed to regulate Sema3A expression. EdU assays, Wound-healing scratch experiments and Transwell migration assays were used to assess VSMC proliferation and migration.
findingsIn this study, we found that semaphorin-3A (Sema3A) was significantly downregulated in VSMCs during neointimal hyperplasia after vascular injury in mice and in human atherosclerotic plaques. Meanwhile, Sema3A was transcriptionally downregulated by PDGF-BB via p53 in VSMCs. Furthermore, we found that overexpression of Sema3A inhibited VSMC proliferation and migration, as well as increasing differentiated gene expression. Mechanistically, Sema3A increased the NRP1-plexin-A1 complex and decreased the NRP1-PDGFRβ complex, thus inhibiting phosphorylation of PDGFRβ. Moreover, we found that overexpression of Sema3A suppressed neointimal hyperplasia after vascular injury in vivo.
interpretationThese results suggest that local delivery of Sema3A may act as a novel therapeutic option to prevent in-stent restenosis.
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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 Socratic graph.