ArticleJournal of molecular neuroscience : MN2019
Oxygen-Glucose Deprivation/Reoxygenation Induces Human Brain Microvascular Endothelial Cell Hyperpermeability Via VE-Cadherin Internalization: Roles of RhoA/ROCK2.
Article in Journal of molecular neuroscience : MN, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- ANGPTL4-dependent metabolic reprogramming fuels RhoA signalling and microvascular dysfunction in diabetes.Acta diabetologica · 2026Article
- Mollugin attenuates oxygen-glucose deprivation/reperfusion-induced brain microvascular endothelial cell death and permeability through activation of BDNF/TrkB-modulated Akt pathway.Journal of bioenergetics and biomembranes · 2025Article
- Diversity of Brain Microvascular Endothelial Cell Functions: Physiology, Ischemia/Hypoxia, and Underlying Protection.Aging and disease · 2025Review
- Total Flavones ofCurrent issues in molecular biology · 2025Article
- The novel ROCK2 selective inhibitor NRL-1049 preserves the blood-brain barrier after acute injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- "Baihui" (DU20)-penetrating "Qubin" (GB7) acupuncture on blood-brain barrier integrity in rat intracerebral hemorrhage models via the RhoA/ROCK II/MLC 2 signaling pathway.Animal models and experimental medicine · 2024Article
- Hydrogen Sulfide Protects against Rat Ischemic Brain Injury by Promoting RhoA Phosphorylation at Serine 188.ACS omega · 2024Article
- Article
- Melanoma Cells Produce Large Vesicular-Bodies That Cause Rapid Disruption of Brain Endothelial Barrier-Integrity and Disassembly of Junctional Proteins.International journal of molecular sciences · 2023Article
- Chlorogenic acid promotes angiogenesis and attenuates apoptosis following cerebral ischaemia-reperfusion injury by regulating the PI3K-Akt signalling.Pharmaceutical biology · 2022Article
- Promising Strategies for the Development of Advanced In Vitro Models with High Predictive Power in Ischaemic Stroke Research.International journal of molecular sciences · 2022Review
- The protective role of raltegravir in experimental acute lung injury in vitro and in vivo.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2022Article
- Study of BBB Dysregulation in Neuropathogenicity Using Integrative Human Model of Blood-Brain Barrier.Frontiers in cellular neuroscience · 2022Review
- Circ_0006768 upregulation attenuates oxygen-glucose deprivation/reoxygenation-induced human brain microvascular endothelial cell injuries by upregulating VEZF1 via miR-222-3p inhibition.Metabolic brain disease · 2021Article
- Deregulated Protein Kinases: Friend and Foe in Ischemic Stroke.Molecular neurobiology · 2021Review
- HCell death discovery · 2021Article
- Salvianolic acid A prevented cerebrovascular endothelial injury caused by acute ischemic stroke through inhibiting the Src signaling pathway.Acta pharmacologica Sinica · 2021Article
- Article
- CD151 Alleviates Early Blood-Brain Barrier Dysfunction After Experimental Focal Brain Ischemia in Rats.Cellular and molecular neurobiology · 2021Article
- Modeling blood-brain barrier pathology in cerebrovascular disease in vitro: current and future paradigms.Fluids and barriers of the CNS · 2020Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The destruction of the blood-brain barrier (BBB) contributes to a spectrum of neurological diseases such as stroke, and the hyperpermeability of endothelial cells is one of the characters of stroke, which is possibly exacerbated after reperfusion. However, the underlying mechanisms involving hyperpermeability after reperfusion between the endothelial cells remain poorly understood. Therefore, in the present study, the human microvascular endothelial cells (HBMECs) were exposed to oxygen-glucose deprivation/reperfusion (OGD/R) to mimic ischemic stroke condition in vitro with the aim to investigate the potential mechanisms induced by OGD/R. The permeability of cultured HBMECs was measured using FITC-labeled dextran in a Transwell system and transendothelial electrical resistance (TEER), while the RhoA activity was detected by pull-down assay. In addition, the phosphorylation of MYPT1, which reflects the activation of ROCK and the internalization of VE-cadherin, was detected by Western blot. It showed that OGD/R treatment significantly increased the permeability of HBMEC monolayers and facilitated the internalization of VE-cadherin in HBMEC monolayers. Pull-down assay showed that RhoA activation was obviously enhanced after OGD/R treatment, while RhoA and ROCK inhibitor significantly reversed OGD/R-induced HBMEC monolayers hyperpermeability and the internalization of VE-cadherin. Meanwhile, the knockdown assay showed that RhoA small interfering RNA (siRNA) led to similar effects. The inactivation of the downstream effector protein ROCK was also examined. Intriguingly, ROCK2 rather than ROCK1 exerted its adverse effects on HBMEC monolayer integrity, since ROCK2 knockdown markedly reverses the injury of OGD/R in HBMEC monolayers. In conclusion, the present study provides evidence that OGD/R may induce HBMEC monolayer hyperpermeability via RhoA/ROCK2-mediated VE-cadherin internalization, which may provide an impetus for the development of therapeutics targeting BBB damage in ischemic stroke.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.