ArticleAmerican journal of translational research2021
NEAT1 promotes the repair of abdominal aortic aneurysms of endothelial progenitor cells via regulating miR-204-5p/Ang-1.
Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Roles and Mechanisms of miRNAs in Abdominal Aortic Aneurysm: Signaling Pathways and Clinical Insights.Current atherosclerosis reports · 2024Review
- Construction of lncRNA- and circRNA-associated ceRNA networks in the prostatic urethra of rats after simulating transurethral laser prostatectomy (TULP).Molecular and cellular biochemistry · 2024Article
- Transcriptomics analysis of long non-coding RNAs in smooth muscle cells from patients with peripheral artery disease and diabetes mellitus.Scientific reports · 2024Article
- The roles of long noncoding RNA NEAT1 in cardiovascular diseases.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo clarify the regulatory effect of Nuclear-enriched abundant transcript 1 (NEAT1) on abdominal aortic aneurysm (AAA) model rats and isolated endothelial progenitor cells (EPCs).
methodsThe AAA rat model was established by CaCl
resultsOverexpressed NEAT1 not only reduced inflammatory infiltration and increased the number of EPCs in abdominal aorta and peripheral blood, but also promoted the viability, migration, tube formation of EPCs, increased VEGF content and upregulated the expression of the Ang-1/ERK pathway in EPCs. However, silencing NEAT1 produced opposite results. NEAT1 targeting miR-204-5p inhibited the functional effects of miR-204-5p on of EPCs. Overexpressed/silencing Ang-1 partially reversed the effects of NEAT1 or miR-204-5p on the characteristics of EPCs.
conclusionNEAT1 competitively binds with miR-204-5p and up-regulates Ang-1 expression in EPCs to effectively improve the proliferation, migration and angiogenesis of EPCs.
Indexed as
Identifiers
34017378PMC8129351W3161296746What OpenQuestion holds
Registered trials
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