ArticleHuman cell2020
LncRNA HCG18 is critical for vascular smooth muscle cell proliferation and phenotypic switching.
Article in Human cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- lncRNA HOTAIR promotes airway remodeling by regulating metabolic reprogramming through the FUS/HK2 axis in airway smooth muscle cells.Molecular biology reports · 2026Article
- Targeting PDGF/PDGFR Signaling Pathway by microRNA, lncRNA, and circRNA for Therapy of Vascular Diseases: A Narrow Review.Biomolecules · 2024Review
- LncRNA HCG18 affects diabetic cardiomyopathy and its association with miR-9-5p/IGF2R axis.Heliyon · 2024Article
- LncRNA HCG18 affects aortic dissection through the miR-103a-3p/HMGA2 axis by modulating proliferation and apoptosis of vascular smoothing muscle cells.Clinics (Sao Paulo, Brazil) · 2024Article
- Establishing a competing endogenous RNA (ceRNA)-immunoregulatory network associated with the progression of Alzheimer's disease.Annals of translational medicine · 2022Article
- Long non-coding RNAs: Modulators of phenotypic transformation in vascular smooth muscle cells.Frontiers in cardiovascular medicine · 2022Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have shown that some specific long non-coding RNAs are dysregulated in vascular walls and abnormally expressed in vascular disease. LncRNA HLA complex group 18 (HCG18) is a member of the HLA complex group, which has been rarely investigated in human diseases. In this study, we aimed to investigate the role of HCG in vascular smooth muscle cells. HCG18 was over-expressed by adenovirus transfection and knocked down in vascular smooth muscle cells by shRNA. Cell proliferation was detected by CCK-8 assays. Flow cytometry was employed to test the impacts of HCG18 on vascular smooth muscle apoptotic cells. The expression of associated genes in protein and mRNA levels was detected by western blotting, immunofluorescence and qRT-PCR. The interactions between HCG18 and fused in sarcoma (FUS) were confirmed by RNA EMSA and RIP assays. The expression of serum HCG18 was decreased in hypertensive patients and PDGF-BB-treated vascular smooth muscle cells. HCG18 inhibited proliferation and induced apoptotic cells in vascular smooth muscle cells. In addition, we also found that HCG18 can inhibit vascular smooth muscle cell phenotypic switching from a contractile to a secretory phenotype. Finally, our results showed that HCG18 enhanced apoptotic cells by directly binding with FUS. Our findings reveal that HCG18 is involved in the regulation of proliferation, apoptosis and the expression levels of markers of the contractile and synthetic phenotype.
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Registered trials
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 OpenQuestion graph.