ArticleNeurochemical research2020
LncRNA MALAT1 Promotes OGD-Induced Apoptosis of Brain Microvascular Endothelial Cells by Sponging miR-126 to Repress PI3K/Akt Signaling Pathway.
Article in Neurochemical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Functional dynamics of lncRNAs and miRNAs in cancer metabolism and neuroinflammation.Molecular biology reports · 2026Review
- Can miRNAs in MSCs-EVs Offer a Potential Treatment for Hypoxic-ischemic Encephalopathy?Stem cell reviews and reports · 2025Review
- LncRNAs and CircRNAs as Strategies against Pathological Conditions Caused by a Hypoxic/Anoxic State.Biomolecules · 2023Review
- RNF7 Induces Skeletal Muscle Cell Apoptosis and Arrests Cell Autophagy via Upregulation of THBS1 and Inactivation of the PI3K/Akt Signaling Pathway in a Rat Sepsis Model.Infection and immunity · 2023Article
- Circvrk1 downregulation attenuates brain microvascular endothelial cell damage induced by oxygen-glucose deprivation through modulating the miR-150-5p/MLLT1 axis.Experimental brain research · 2023Article
- Partial Synthetic PPARƳ Derivative Ameliorates Aorta Injury in Experimental Diabetic Rats Mediated by Activation of miR-126-5p Pi3k/AKT/PDK 1/mTOR Expression.Pharmaceuticals (Basel, Switzerland) · 2022Article
- MicroRNA-223 Attenuates Stretch-Injury-Induced Apoptosis in Brain Microvascular Endothelial Cells by Regulating RhoB Expression.Brain sciences · 2022Article
- Stress conditions induced circRNAs profile of extracellular vesicles in brain microvascular endothelial cells.Metabolic brain disease · 2022Article
- An update on the functional roles of long non‑coding RNAs in ischemic injury (Review).International journal of molecular medicine · 2022Review
- Advances and Challenges in Biomarkers Use for Coronary Microvascular Dysfunction: From Bench to Clinical Practice.Journal of clinical medicine · 2022Review
- Article
- Long Non Coding RNA Based Regulation of Cerebrovascular Endothelium.Frontiers in genetics · 2022Review
- The mechanisms of glycolipid metabolism disorder on vascular injury in type 2 diabetes.Frontiers in physiology · 2022Review
- Role of lncRNAs in the Development of Ischemic Stroke and Their Therapeutic Potential.Molecular neurobiology · 2021Review
- The Regulatory Functions of lncRNAs on Angiogenesis Following Ischemic Stroke.Frontiers in molecular neuroscience · 2020Review
- Transcription Factor E2F1 Aggravates Neurological Injury in Ischemic Stroke via microRNA-122-Targeted Sprouty2.Neuropsychiatric disease and treatment · 2020Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Ischemic stroke (IS) is a common disease that seriously endangers human health. Patients with IS present with increased death of brain microvascular endothelial cells (BMECs). MALAT1 is found to be upregulated in IS patients. However, the function of MALAT1 in IS pathogenesis still remains unclear. This study aimed to investigate the role of MALAT1 in IS in vitro model and the related molecular mechanisms. The expressions of MALAT1 and miR-126 were detected by qPCR. The in vitro IS model was established by treating BMECs with oxygen-glucose deprivation (OGD). Cell viability and cell apoptosis were assessed by MTT assay and flow cytometry, respectively. Luciferase assay was conducted to examine the interplay between MALAT1 and miR-126. Western blotting was used to determine the protein levels of apoptosis-associated proteins (e.g. caspase 3, Bax and Bcl-2) and PI3K/Akt pathway-related proteins (e.g. PI3K, Akt, p-PI3K, p-Akt). OGD induced upregulation of MALAT1 and downregulation of miR-126 in HBMECs. MALAT1 knockdown promoted the proliferation of HBMECs and reduced the proportion of apoptotic HBMECs by regulating the expression of apoptosis-related proteins. MALAT1 targeted and negatively regulated miR-126 expression. Overexpression of miR-126 activated the PI3K/Akt pathway, which in turn affected the proliferation and apoptosis of HBMECs. MALAT1 negatively regulated PI3K/Akt pathway. MALAT1 inhibited the proliferation and induced the apoptosis of OGD-induced HBMECs through suppressing PI3K/AKT pathway by sponging miR-126, providing a potential therapeutic target for IS.
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Registered trials
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