ArticleExperimental and therapeutic medicine2017
MicroRNA-138 inhibits hypoxia-induced proliferation of endothelial progenitor cells via inhibition of HIF-1α-mediated MAPK and AKT signaling.
Article in Experimental and therapeutic medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 12 papers.
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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.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Non-Coding RNAs as Potential Diagnostic/Prognostic Markers for Hepatocellular Carcinoma.International journal of molecular sciences · 2024Review
- MicroRNA-126 and VEGF enhance the function of endothelial progenitor cells in acute myocardial infarction.Experimental and therapeutic medicine · 2022Article
- miR-138-5p Inhibits Vascular Mimicry by Targeting the HIF-1Journal of immunology research · 2022Article
- Aberrant expression of miR-138 as a novel diagnostic biomarker in systemic sclerosis.Biomarker insights · 2022Article
- Review
- MicroRNA-138-1-3p sensitizes sorafenib to hepatocellular carcinoma by targeting PAK5 mediated β-catenin/ABCB1 signaling pathway.Journal of biomedical science · 2021Article
- Sevoflurane Postconditioning Attenuates Hypoxia/Reoxygenation Injury of Cardiomyocytes Under High Glucose by Regulating HIF-1α/MIF/AMPK Pathway.Frontiers in pharmacology · 2020Article
- A perspective on the diagnostics, prognostics, and therapeutics of microRNAs of triple-negative breast cancer.Biophysical reviews · 2019Review
- Exercise and Cardiovascular Progenitor Cells.Comprehensive Physiology · 2019Review
- Exogenous FGF-2 improves biological activity of endothelial progenitor cells exposed to high glucose conditions.Journal of interventional medicine · 2018Article
- MicroRNA-126 Priming Enhances Functions of Endothelial Progenitor Cells under Physiological and Hypoxic Conditions and Their Therapeutic Efficacy in Cerebral Ischemic Damage.Stem cells international · 2018Article
- Critical effects of epigenetic regulation in pulmonary arterial hypertension.Cellular and molecular life sciences : CMLS · 2017Review
Corrections and comments
- Retraction · 2021-07-14Author Unresponsive · Concerns/Issues about Data · Duplication of/in Image · Investigation by Third Party · Paper Mill · · see also: https://pubpeer.com/publications/E6E47BB87CF88E6AFB7421002E5CDC
- Retracted
- Retracted
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelial progenitor cells (EPCs) participate in angiogenesis by differentiating into endothelial cells (ECs) and may be developed to treat ischemia/reperfusion injury. MicroRNAs (miRs) are a type of non-coding RNA that are 18-25 nucleotides in length and serve a role in angiogenesis. It has been demonstrated that miR-138 regulates hypoxia-induced EC dysfunction. However, to the best of our knowledge, the exact role of miR-138 in the regulation of hypoxia-induced EPCs has not previously been reported. In the present study, data collected from an MTT assay indicated that hypoxia treatment enhanced EPC proliferation, which was accompanied by an upregulation of hypoxia-inducible factor 1α (HIF-1α) expression. miR-138 overexpression inhibited hypoxia-induced EPC proliferation and induced cell cycle arrest at the G1 stage. A mechanistic investigation revealed that miR-138 negatively regulated HIF-1α protein levels but did not affect HIF-1α mRNA levels in EPCs. Moreover, results from a dual luciferase reporter assay demonstrated that HIF-1α was a direct target of miR-138 in EPCs. Furthermore, upregulation of miR-138 suppressed the hypoxia-induced upregulation of HIF-1α. Downstream factors of HIF-1α were also investigated and it was observed that the upregulation of miR-138 inhibited the hypoxia-induced upregulation of vascular endothelial growth factor, as well as the activity of mitogen-activated protein kinase and AKT signaling in EPCs. In summary, the present study suggested that miR-138 inhibits hypoxia-induced EPC proliferation, possibly by inhibiting HIF-1α-mediated signaling.
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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.