ArticleAging2020
HIX003209 promotes vascular smooth muscle cell migration and proliferation through modulating miR-6089.
Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Targeting PDGF/PDGFR Signaling Pathway by microRNA, lncRNA, and circRNA for Therapy of Vascular Diseases: A Narrow Review.Biomolecules · 2024Review
- miR-6089 may prevent the inflammatory events leading to cardiovascular disorders in RA patients.Heliyon · 2024Article
- The Effect of TNF-Cardiology research and practice · 2022Review
- Article
- Dysregulated long non-coding RNAs involved in regulation of matrix degradation during type-B aortic dissection pathogenesis.General thoracic and cardiovascular surgery · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating references have showed that long noncoding RNAs (lncRNAs) act important roles in the development of human diseases. The role and expression of HIX003209 remains unclear in the pathogenesis of atherosclerosis. We showed that HIX003209 expression was upregulated in atherosclerotic coronary tissues compared to normal coronary artery samples. HIX003209 was overexpressed in vascular smooth muscle cells (VSMCs) induced by inflammatory mediators including tumor necrosis factor-α(TNF-α), ox-LDL and latelet-derived growth factor-BB (PDGF-BB). Ectopic expression of HIX003209 enhanced cell growth and migration and induced inflammatory mediators secretion such as interleukin 6 (IL-6), TNF-α and IL-1β in VSMCs. Furthermore, we showed that miR-6089 was downregulated in atherosclerotic coronary tissues compared to normal coronary artery samples. There was a negative association between expression of HIX003209 and miR-6089 in atherosclerotic coronary tissues. MiR-6089 expression was decreased in VSMCs induced by inflammatory mediators including TNF-α, ox-LDL and PDGF-BB. Dual luciferase analysis showed that miR-6089 overexpression decreased luciferase activity of HIX003209 WT-type 3'-UTR but not the mut-type 3'-UTR. Overexpression of HIX003209 suppressed the expression of miR-6089 in VSMCs. Ectopic expression of HIX003209 induced cell growth, migration and the secretion of inflammatory mediators via regulating miR-6089 expression. These data suggested that HIX003209 promoted VSMCs proliferation, migration and the secretion of inflammatory mediators partly via regulating miR-6089.
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What OpenQuestion holds
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.