ArticleMetabolic brain disease2022
LncRNA SNHG14 is beneficial to oxygen glucose deprivation/reoxygenation-induced neuro-2a cell injury via mir-98-5p sequestration-caused BCL2L13 upregulation.
Article in Metabolic brain disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 13 citations in OpenAlex.
- METTL3 Confers Ischemia/Reperfusion-Caused Myocardial Injury by Triggering Ferroptosis via Regulating the lncRNA SNHG14/miR-195a-5p/ACSL4 Axis.Cardiovascular drugs and therapy · 2026Article
- Downregulation of lncRNA SNHG14 Alleviates Neuropathic Pain and Inflammation in CCI Rats by Targeting miR-182-5p/BDNF.Neurochemical research · 2026Article
- Effects and mechanisms of synovial mesenchymal stem cell-derived extracellular vesicular LncRNA-SNHG14 on chondrocyte injury.Regenerative therapy · 2026Article
- LncRNA SNHG14 Regulates the Expression of BDNF by Recruiting Histone Methyltransferase EZH2 to Mediate H3K27me3, Thereby Affecting Angiogenesis and Functional Recovery After Cerebral Ischemia.Molecular neurobiology · 2025Article
- Values of LncRNA SNHG14 in the Differential Diagnosis and Prognosis Evaluation of Acute Ischemic Stroke.Applied biochemistry and biotechnology · 2025Article
- LncRNA-driven programmed cell death networks: new therapeutic targets for neurological disorders.Frontiers in molecular neuroscience · 2025Review
- LncRNA SNHG14 silencing attenuates the progression of diabetic nephropathy via the miR-30e-5p/SOX4 axis.Journal of diabetes · 2024Article
- Molecular Characterization and Expression Changes of theCurrent issues in molecular biology · 2024Article
- LncRNAs and CircRNAs as Strategies against Pathological Conditions Caused by a Hypoxic/Anoxic State.Biomolecules · 2023Review
- The Role of microRNAs in Epigenetic Regulation of Signaling Pathways in Neurological Pathologies.International journal of molecular sciences · 2023Review
- Biological properties of the BCL-2 family protein BCL-RAMBO, which regulates apoptosis, mitochondrial fragmentation, and mitophagy.Frontiers in cell and developmental biology · 2022Review
- Early diagnosis value of lncRNA SNHG14 combined with miR-493-5p in gestational diabetes mellitus and its correlation with pregnancy outcome.Diabetes & vascular disease researchArticle
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe deregulation of long non-coding RNA (lncRNA) is associated with diverse human disorders, including cerebral ischemia/reperfusion injury (CI/RI). LncRNA SNHG14 was reported to function in CI/RI. Whereas, molecular mechanisms regulated by SNHG14 are not fully unveiled.
methodsMice subjected to middle cerebral artery occlusion/reperfusion (MCAO/R) were used as CI/RI animal models. Neuro-2a (N2A) cells subjected to oxygen glucose deprivation/reoxygenation (OGD/R) were used as CI/RI cell models. The expression of SNHG14, miR-98-5p and BCL2 like 13 (BCL2L13) was examined using quantitative real-time PCR (qPCR) or western blot. Apoptosis was monitored by flow cytometry assay. Apoptosis-related markers and endoplasmic reticulum (ER) stress-related markers were quantified by western blot. Inflammatory factors and oxidative stress were detected using matched commercial kits. The predicted relationship between miR-98-5p and SNHG14 or BCL2L13 was validated by dual-luciferase reporter assay, RIP assay and pull-down assay.
resultsThe high expression of SNHG14 was monitored in MCAO/R-treated mice and OGD/R-treated N2A cells. OGD/R-induced N2A cell apoptosis, ER stress, inflammation and oxidative stress were attenuated by SNHG14 knockdown. SNHG14 targeted miR-98-5p to positively regulate BCL2L13 expression. Inhibition of miR-98-5p recovered cell apoptosis, ER stress, inflammation and oxidative stress that were repressed by SNHG14 knockdown. Overexpression of BCL2L13 enhanced cell apoptosis, ER stress, inflammation and oxidative stress that were repressed by miR-98-5p enrichment.
conclusionsSNHG14 knockdown alleviated OGD/induced N2A cell apoptosis, ER stress, inflammation and oxidative stress by depleting BCL2L13 via increasing miR-98-5p.
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