ArticleMolecular medicine reports2020
Long non‑coding RNA SNHG16 inhibits the oxygen‑glucose deprivation and reoxygenation‑induced apoptosis in human brain microvascular endothelial cells by regulating miR‑15a‑5p/bcl‑2.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Dysregulated MicroRNAs in Parkinson's Disease: Pathogenic Mechanisms and Biomarker Potential.International journal of molecular sciences · 2026Article
- Targeting the proliferation of glioblastoma cells and enhancement of doxorubicin and temozolomide cytotoxicity through inhibition of PFKFB4 and HMOX1 genes with siRNAs.Scientific reports · 2025Article
- LncRNA SNHG16 Inhibits IntracellularACS omega · 2024Article
- Identification of mitophagy-related hub genes during the progression of spinal cord injury by integrated multinomial bioinformatics analysis.Biochemistry and biophysics reports · 2024Article
- LncRNAs and CircRNAs as Strategies against Pathological Conditions Caused by a Hypoxic/Anoxic State.Biomolecules · 2023Review
- Exploring Circulating Long Non-Coding RNAs in Mild Cognitive Impairment Patients' Blood.Biomedicines · 2023Article
- MiR-15a-5p accelerated vascular smooth muscle cells viabilities and migratory abilities via targeting Bcl-2.Physiological research · 2022Article
- The correlation of lncRNA SNHG16 with inflammatory cytokines, adhesion molecules, disease severity, and prognosis in acute ischemic stroke patients.Journal of clinical laboratory analysis · 2022Article
- Mechanism of lncRNA SNHG16 in oxidative stress and inflammation in oxygen-glucose deprivation and reoxygenation-induced SK-N-SH cells.Bioengineered · 2022Article
- A narrative review of long noncoding RNA: insight into neural ischemia/reperfusion mediated by two pathophysiological processes of injury and repair.Annals of translational medicine · 2022Review
- Long Non Coding RNA Based Regulation of Cerebrovascular Endothelium.Frontiers in genetics · 2022Review
- Long non-coding RNA Gm11974 aggravates oxygen-glucose deprivation-induced injury via miR-122-5p/SEMA3A axis in ischaemic stroke.Metabolic brain disease · 2021Article
- Long Non-Coding RNA-Mediated Competing Endogenous RNA Networks in Ischemic Stroke: Molecular Mechanisms, Therapeutic Implications, and Challenges.Frontiers in pharmacology · 2021Review
- The Regulatory Functions of lncRNAs on Angiogenesis Following Ischemic Stroke.Frontiers in molecular neuroscience · 2020Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNA (miR) 15a‑5p can promote ischemia/reperfusion (I/R)‑induced apoptosis of cerebral vascular endothelial cells, which is inhibited by long non‑coding RNAs (lncRNAs). The present study investigated the potential of lncRNAs targeting miR‑15a‑5p to regulate oxygen‑glucose deprivation and reoxygenation (OGD‑R)‑induced apoptosis of human brain microvascular endothelial cells (hBMECs). hBMECs were transfected with or without miR‑15a‑5p or its mutant, together with p‑small nucleolar RNA host gene 16 (SNHG16) or its mutant. Following OGD‑R, proliferation, apoptosis and miR‑15a‑5p, SNHG16 and Bcl‑2 expression levels were determined using MTT, flow cytometry, reverse transcription‑quantitative PCR or western blotting. The potential interaction of SNHG16 with miR‑15a‑5p was analyzed by pull‑down, luciferase and immunoprecipitation assays. OGD‑R induced apoptosis of hBMECs and increased miR‑15a‑5p expression levels in a time‑dependent manner. miR‑15a‑5p overexpression decreased the proliferation of hBMECs and promoted apoptosis by decreasing Bcl‑2 expression levels. SNHG16 was pulled‑down by miR‑15a‑5p and anti‑Ago2. miR‑15a‑5p overexpression significantly decreased SNHG16‑regulated luciferase activity and hBMEC survival by increasing apoptosis. SNHG16 overexpression decreased miR‑15a‑5p expression levels in hBMECs. SNHG16 gradually decreased following OGD‑R and its overexpression decreased miR‑15a‑5p expression levels and promoted the proliferation of hBMECs by decreasing apoptosis. SNHG16 enhanced Bcl‑2 expression levels in hBMECs, which was abrogated by miR‑15a‑5p. Bioinformatics suggest that SNHG16 may antagonize the binding of miR‑15a‑5p to the 3'UTR of Bcl‑2 mRNA. These findings suggest that SNHG16 may protect hBMECs from OGD‑R‑induced apoptosis by antagonizing the miR‑15a‑5p/bcl‑2 axis. Thus, targeting SNHG16‑based mechanisms may provide novel therapeutic strategies for treatment of ischemic stroke.
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