ArticleJournal of bioenergetics and biomembranes2020
The lncRNA FAL1 protects against hypoxia-reoxygenation- induced brain endothelial damages through regulating PAK1.
Article in Journal of bioenergetics and biomembranes, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Exosomal lncRNAs in Cerebrovascular Diseases: Biomarkers, Pathological Mechanisms, and Therapeutic Potential.Non-coding RNA · 2026Review
- LncRNAs and CircRNAs as Strategies against Pathological Conditions Caused by a Hypoxic/Anoxic State.Biomolecules · 2023Review
- Phosphoenolpyruvate induces endothelial dysfunction and cell senescence through stimulation of metabolic reprogramming.Journal of bioenergetics and biomembranes · 2023Article
- Circ VRK1/microRNA-17/PTEN axis modulates the angiogenesis of human brain microvascular endothelial cells to affect injury induced by oxygen-glucose deprivation/reperfusion.BMC neuroscience · 2023Article
- p21-activated kinase 1 (PAK1) as a therapeutic target for cardiotoxicity.Archives of toxicology · 2022Review
- Long Non-coding RNAs (lncRNAs), A New Target in Stroke.Cellular and molecular neurobiology · 2022Review
- Long Non Coding RNA Based Regulation of Cerebrovascular Endothelium.Frontiers in genetics · 2022Review
- The Expanding Regulatory Mechanisms and Cellular Functions of Long Non-coding RNAs (lncRNAs) in Neuroinflammation.Molecular neurobiology · 2021Review
- Emerging Role of LncRNAs in Ischemic Stroke-Novel Insights into the Regulation of Inflammation.Journal of inflammation research · 2021Review
- LncRNAs Stand as Potent Biomarkers and Therapeutic Targets for Stroke.Frontiers in aging neuroscience · 2020Review
- The Regulatory Functions of lncRNAs on Angiogenesis Following Ischemic Stroke.Frontiers in molecular neuroscience · 2020Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulation of cerebral microvascular endothelial cells plays an important role in the pathogenesis of stroke. However, the underlying mechanisms still need to be elucidated. In the current study, we found that the long non-coding RNA (lncRNA) FAL1 was significantly reduced in response to oxygen-glucose deprivation and reoxygenation (OGD/R) stimulation in human primary brain microvascular endothelial cells (HBMVECs). Interestingly, overexpression of FAL1 ameliorated OGD/R-induced oxidative stress by reducing the production of reactive oxygen species (ROS) and increasing the level of reduced glutathione (GSH). Also, overexpression of FAL1 suppressed OGD/R-induced secretions of interleukin-6 (IL-6), monocyte chemotactic protein-1 (MCP-1), and high mobility group box-1 (HMGB-1). We then found that OGD/R-induced reduction of cell viability and release of lactate dehydrogenase (LDH) were prevented by overexpression of FAL1. Additionally, exposure to OGD/R significantly reduced the phosphorylated levels of PAK1 and AKT as well as the total level of proliferating cell nuclear antigen (PCNA), which was restored by overexpression of FAL1. Importantly, overexpression of FAL1 restored OGD/R-induced reduction in the expression of endothelial nitric oxide synthase (eNOS) and the subsequent release of nitric oxide (NO). Our results implicate that FAL1 might be involved in the process of brain endothelial cell damage.
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