AI Article Synopsis

  • Dysregulation of cerebral microvascular endothelial cells contributes to stroke, and this study investigates the role of the long non-coding RNA (lncRNA) FAL1 in this context.
  • The researchers observed that FAL1 levels decrease following oxygen-glucose deprivation and reoxygenation (OGD/R) stress, but overexpressing FAL1 can reduce oxidative stress and inflammation in brain cells.
  • Additionally, FAL1 overexpression helps maintain cell viability, restores key cellular functions, and counteracts damage related to stroke, suggesting its potential protective role in brain endothelial cell health.

Article 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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http://dx.doi.org/10.1007/s10863-019-09819-2DOI Listing

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Article Synopsis
  • Dysregulation of cerebral microvascular endothelial cells contributes to stroke, and this study investigates the role of the long non-coding RNA (lncRNA) FAL1 in this context.
  • The researchers observed that FAL1 levels decrease following oxygen-glucose deprivation and reoxygenation (OGD/R) stress, but overexpressing FAL1 can reduce oxidative stress and inflammation in brain cells.
  • Additionally, FAL1 overexpression helps maintain cell viability, restores key cellular functions, and counteracts damage related to stroke, suggesting its potential protective role in brain endothelial cell health.
View Article and Find Full Text PDF

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