ArticleComputational and mathematical methods in medicine2021
MiR-429 Inhibits the Angiogenesis of Human Brain Microvascular Endothelial Cells through SNAI2-Mediated GSK-3
Article in Computational and mathematical methods in medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Harnessing miRNA therapeutics: a novel approach to combat heart and brain infarctions in atherosclerosis.Cell death discovery · 2025Review
- 5-Methoxytryptophan improves cerebrovascular injury induced by chronic kidney disease through NF-κB pathway.In vitro cellular & developmental biology. Animal · 2025Article
- Mir‑429 and GATA4 May Participate in Cerebral Ischemic Stroke by Regulating Autophagy and Apoptosis: the Impact of Chlorogenic Acid.Archives of Razi Institute · 2025Article
- Non-coding RNAs and angiogenesis in cardiovascular diseases: a comprehensive review.Molecular and cellular biochemistry · 2024Review
- Identification and analysis of key immunity-related genes in experimental ischemic stroke.Heliyon · 2024Article
- Mechanisms of Postischemic Stroke Angiogenesis: A Multifaceted Approach.Journal of inflammation research · 2024Review
- HIF-1-Induced hsa-miR-429: Understanding Its Direct Targets as the Key to Developing Cancer Diagnostics and Therapies.Cancers · 2023Review
- Genome-Wide Studies in Ischaemic Stroke: Are Genetics Only Useful for Finding Genes?International journal of molecular sciences · 2022Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNA (miRNA) dysfunction has been confirmed as a key event of ischemic stroke appearance. This study is aimed at revealing the role of miR-429 in the angiogenesis of HBMECs. The HBMECs were treated with oxygen and glucose deprivation (OGD) to establish the ischemic cell model. The qRT-PCR was used to measure the expression levels of the miR-429 in the serums of the patients or cells, and CCK-8, wound healing assay, and tube formation assay were used to observe the effects of miR-429 on the phenotype of HBMECs. Moreover, the Targetscan, dual-luciferase reporter assay, and Western blot were used to reveal the downstream target and regulation mechanism of miR-429 in OGD-induced HBMECs. The results showed that miR-429 was significantly upregulated in the serums of the patients, and overexpressed miR-429 could extremely inhibit the viability, migration, and tube formation of OGD-induced HBMECs. Furthermore, it was found that SNAI2 was a downstream factor of miR-429, and SNAI2 could rescue the effects of miR-429 on OGD-induced HBMECs. Besides, the Western blot showed that miR-429 could affect the activity of GSK-3
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