ArticleCell cycle (Georgetown, Tex.)2021
Long non-coding RNA NORAD induces phenotypic regulation of vascular smooth muscle cells through regulating microRNA-136-5p-targeted KDM1A.
Article in Cell cycle (Georgetown, Tex.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Epigenetic mechanisms in aneurysm formation, growth, and rupture: A systematic review.Interventional neuroradiology : journal of peritherapeutic neuroradiology, surgical procedures and related neurosciences · 2025Review
- LncRNA PVT1 Facilitates Phenotypic Switching of Vascular Smooth Muscle Cells in Intracranial Aneurysms by Recruiting KDM1A to Reduce H3K9me2 Modification.The Kaohsiung journal of medical sciences · 2025Article
- Intracranial Aneurysm Biomarkers: A Convergence of Genetics, Inflammation, Oxidative Stress, and the Extracellular Matrix.International journal of molecular sciences · 2025Review
- Molecular Mechanisms and Roles of MiR-136-5p in Human Cancer and Other Disorders.Current medicinal chemistry · 2025Review
- Prospective Study of lncRNA NORAD for Predicting Cerebrovascular Events in Asymptomatic Patients with Carotid Artery Stenosis.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisArticle
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveEffect of long non-coding RNAs (lncRNAs) on intracranial aneurysm (IA) development has been identified, while the role of noncoding RNA activated by DNA damage (NORAD) in IA remains unexplored. We aimed to verify the impact of NORAD on IA through sponging microRNA-136-5p (miR-136-5p).
methodsRuptured and unruptured IAs were harvested from IA patients, and expression of NORAD, miR-136-5p, and KDM1A was determined. The vascular smooth muscle cells (VSMCs) were cultured and, respectively, transfected with altered NORAD, miR-136-5p, or lysine-specific demethylase 1 (KDM1A) to observe their effect on biological functions, as well as on contraction and synthesis-specific indices of VSMCs. Interactions between NORAD and miR-136-5p, and between miR-136-5p and KDM1A were confirmed.
resultsNORAD and KDM1A were upregulated while miR-136-5p was downregulated in IA, especially in ruptured IA. NORAD overexpression or miR-136-5p inhibition accelerated proliferation and migration, and decelerated phenotypic switching and apoptosis of VSMCs. The effects of overexpressed NORAD on VSMCs were reserved by miR-136-5p upregulation or KDM1A knockdown. NORAD functioned as a competing endogenous RNA of miR-136-5p and miR-136-5p targeted KDM1A.
conclusionNORAD suppressed miR-136-5p, thus upregulating KDM1A to participate in IA formation and rupture by inducing phenotypic regulation of VSMCs.
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