ArticleJournal of cellular and molecular medicine2019
Long non-coding RNA SNHG16 regulates human aortic smooth muscle cell proliferation and migration via sponging miR-205 and modulating Smad2.
Article in Journal of cellular and molecular medicine, 2019. 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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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Dysregulated lncRNAs are associated with the progressive arterial phenotype in Hutchinson-Gilford Progeria Syndrome.GeroScience · 2026Article
- Targeting PDGF/PDGFR Signaling Pathway by microRNA, lncRNA, and circRNA for Therapy of Vascular Diseases: A Narrow Review.Biomolecules · 2024Review
- The correlation of lncRNA SNHG16 with inflammatory cytokines, adhesion molecules, disease severity, and prognosis in acute ischemic stroke patients.Journal of clinical laboratory analysis · 2022Article
- Article
- The Combined Regulation of Long Non-coding RNA and RNA-Binding Proteins in Atherosclerosis.Frontiers in cardiovascular medicine · 2021Review
- Unveiling the ups and downs of miR-205 in physiology and cancer: transcriptional and post-transcriptional mechanisms.Cell death & disease · 2020Review
- Breast cancer-derived exosomes transmit lncRNA SNHG16 to induce CD73+γδ1 Treg cells.Signal transduction and targeted therapy · 2020Article
- SNHG1 Inhibits ox-LDL-Induced Inflammatory Response and Apoptosis of HUVECsFrontiers in pharmacology · 2020Article
- Long non-coding RNA SNHG16 regulates human aortic smooth muscle cell proliferation and migration via sponging miR-205 and modulating Smad2.Journal of cellular and molecular medicine · 2019Article
- Silencing MMP2-AS1 inhibits the proliferation and migration of endothelial cells via YB-1.Science progressArticle
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study investigated the role of long non-coding RNA (lncRNA) small nucleolar RNA host gene 16 (SNHG16) in the human aortic smooth muscle cell (HASMC) proliferation and migration and explored the potential link between SNHG16 and atherosclerosis. Our results showed that platelet-derived growth factor (PDGF)-bb treatment promoted cell proliferation and migration with concurrent up-regulation of SNHG16 in HASMCs. Small nucleolar RNA host gene 16 overexpression promoted HASMC proliferation and migration, while SNHG16 knockdown suppressed cell proliferation and migration in PDGF-bb-stimulated HASMCs. The bioinformatic analyses showed that SNHG16 possessed the complementary binding sequence with miR-205, where the interaction was confirmed by luciferase reporter assay and RNA pull-down assay in HASMCs, and SNHG16 inversely regulated miR-205 expression. MiR-205 overexpression attenuated the enhanced effects of PDGF-bb treatment on HASMC proliferation and migration. Moreover, Smad2 was targeted and inversely regulated by miR-205, while being positively regulated by SNHG16 in HASMCs. Smad2 knockdown attenuated PDGF-bb-mediated actions on HASMC proliferation and migration. Both miR-205 overexpression and Smad2 knockdown partially reversed the effects of SNHG16 overexpression on HASMC proliferation and migration. Moreover, SNHG16 and Smad2 mRNA were up-regulated, while miR-205 was down-regulated in the plasma from patients with atherosclerosis. Small nucleolar RNA host gene 16 expression was inversely correlated with miR-205 expression and positively correlated with Smad2 expression in the plasma from atherosclerotic patients. In conclusion, our data showed the up-regulation of SNHG16 in pathogenic-stimulated HASMCs and clinical samples from atherosclerotic patients. Small nucleolar RNA host gene 16 regulated HASMC proliferation and migration possibly via regulating Smad2 expression by acting as a competing endogenous RNA for miR-205.
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