ArticleJournal of the American Heart Association2020
Smad3 Regulates Neuropilin 2 Transcription by Binding to its 5' Untranslated Region.
Article in Journal of the American Heart Association, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- NovelbioRxiv : the preprint server for biology · 2026Article
- Neuropilin-2 upregulation by stromal TGFβ1 induces lung disseminated tumor cells dormancy escape and promotes metastasis outgrowth.Neoplasia (New York, N.Y.) · 2025Article
- Clusters of mammalian conserved RNA structures in UTRs associate with RBP binding sites.NAR genomics and bioinformatics · 2024Article
- Orchestrating Resilience: How Neuropilin-2 and Macrophages Contribute to Cardiothoracic Disease.Journal of clinical medicine · 2024Review
- The role of 6-phosphogluconate dehydrogenase in vascular smooth muscle cell phenotypic switching and angioplasty-induced intimal hyperplasia.JVS-vascular science · 2024Article
- Impact of the transforming growth factor-β pathway on vascular restenosis and its mechanism.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023Article
- Non-coding RNAs are key players and promising therapeutic targets in atherosclerosis.Frontiers in cell and developmental biology · 2023Review
- Angioplasty induces epigenomic remodeling in injured arteries.Life science alliance · 2022Article
- Emerging Roles for Neuropilin-2 in Cardiovascular Disease.International journal of molecular sciences · 2020Review
- Smad3 Regulates Neuropilin 2 Transcription by Binding to its 5' Untranslated Region.Journal of the American Heart Association · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Background Vascular smooth muscle cell phenotypic change and consequential intimal hyperplasia (IH) cause arterial stenosis and posttreatment restenosis. Smad3 is a master transcription factor, yet its underlying functional mechanisms in this disease context are not well defined. Methods and Results In cultured smooth muscle cells, Smad3 silencing and overexpression respectively reduced and increased the mRNA and protein of NRP2 (neuropilin 2), a recently reported pro-IH signaling factor. Smad3 silencing attenuated pro-IH smooth muscle cell phenotypes including proliferation, migration, and dedifferentiation (reduced smooth muscle α-actin). While increased Smad3 enhanced these phenotypes, NRP2 silencing abolished this enhancement. Interestingly, the 5' untranslated region but not the promoter of NRP2 was indispensable for Smad3-enhanced transcriptional activity (luciferase assay); both chromatin immunoprecipitation and electrophoretic mobility shift assay showed predominant Smad3 binding in the +51 to +78 bp region of NRP2's 5' untranslated region. In vivo, Smad3 haploinsufficiency reduced NRP2 (immunostaining) and IH (by 47%) in wire-injured mouse femoral arteries. Conclusions Smad3 controls NRP2 expression by occupying its 5' untranslated region in promoting smooth muscle cell phenotypic change in vitro. This and in vivo results shed new light on the long-debated role of Smad3 in IH.
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