ArticleInternational journal of clinical and experimental pathology2019
The upregulation of miR-101 promotes vascular endothelial cell apoptosis and suppresses cell migration in acute coronary syndrome by targeting CDH5.
Article in International journal of clinical and experimental pathology, 2019. 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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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Article
- Hypoxia-Induced miR-101 Impairs Endothelial Barrier Integrity Through Altering VE-Cadherin and Claudin-5.Molecular neurobiology · 2024Article
- CTRP15 promotes macrophage cholesterol efflux and attenuates atherosclerosis by increasing the expression of ABCA1.Journal of physiology and biochemistry · 2022Article
- Melatonin upregulates DNA-PKcs to suppress apoptosis of human umbilical vein endothelial cells via inhibiting miR-101 under HMolecular and cellular biochemistry · 2021Article
- Upregulation of Serum miRNA-3615 Serves as a Biomarker to Predict Disease Onset and Prognosis in Acute Coronary Syndrome Patients.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisArticle
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRNAs) have been reported to be of great importance in a wide range of physiological and pathological processes, including acute coronary syndrome (ACS). However, the exact role of miRNAs in the pathogenesis of ACS has not been fully elucidated. In this study, we found that miR-101 was significantly upregulated in the serum samples of patients with acute coronary syndrome compared with healthy controls. In human umbilical vein endothelial cells (HUVECs), the overexpression of miR-101 drastically promoted cell apoptosis and inhibited cell migration. Mechanistically, miR-101 repressed the expression of CHD5 by targeting its 3'-untranslated region (3'UTR). The silencing of CHD5 also induced cell apoptosis and suppressed cell migration in HUVECs. Taken together, our findings suggest that the miR-101-CHD5 axis may play an important role in the biological behaviors of endothelial cells during the pathogenesis of ACS and may afford an effective diagnostic marker and a powerful therapy for this disease.
Indexed as
Identifiers
31934175PMC6949823W3026883360What OpenQuestion holds
Registered trials
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