ArticleMolecular biology reports2024
Up-regulation of miR-126 via DNA methylation in hypoxia-preconditioned endothelial cells may contribute to hypoxic tolerance of neuronal cells.
Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed.
- Mechanical pressure on endothelial cells mediates remote ischaemic preconditioning-induced neuroprotection via miR-126.Experimental physiology · 2026Article
- High-altitude hypoxic cues and cerebral ischemic tolerance: an evidence-graded translational framework for stroke research.Frontiers in neuroscience · 2026Review
- MicroRNA-126 as an endogenous molecule for hypoxic/ischemic tolerance in neuroprotection.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Review
- Hypoxic preconditioning modulates BDNF signaling to alleviate depression-like behaviors in mice and its whole transcriptome sequencing analysis.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
backgroundEndothelial cells (ECs) can confer neuroprotection by secreting molecules. This study aimed to investigate whether DNA methylation contributes to the neuroprotective gene expression induced by hypoxia preconditioning (HPC) in ECs and to clarify that the secretion of molecules from HPC ECs may be one of the molecular mechanisms of neuroprotection.
methodsHuman microvascular endothelial cell-1 (HMEC-1) was cultured under normal conditions (C), hypoxia(H), and hypoxia preconditioning (HPC), followed by the isolation of culture medium (CM). SY5Y cell incubated with the isolated CM from HMEC-1 was exposed to oxygen-glucose deprivation (OGD). The DNA methyltransferases (DNMTs), global methylation level, miR-126 and its promotor DNA methylation level in HMEC-1 were measured. The cell viability and cell injury in SY5Y were detected.
resultsHPC decreased DNMTs level and global methylation level as well as increased miR-126 expression in HMEC-1. CM from HPC treated HMEC-1 also relieved SY5Y cell damage, while CM from HMEC-1 which over-expression of miR-126 can reduce injury in SY5Y under OGD condition.
conclusionsThese findings indicate EC may secrete molecules, such as miR-126, to execute neuroprotection induced by HPC through regulating the expression of DNMTs.
Indexed as
Identifiers
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Registered trials
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