ArticleThe Biochemical journal2002
Extracellular signal-regulated protein kinase activation during reoxygenation is required to restore ischaemia-induced endothelial barrier failure.
Article in The Biochemical journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 49 citations in OpenAlex.
- High-density lipoproteins limit neutrophil-induced damage to the blood-brain barrier in vitro.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2013Trial
- Vitexin reduces epilepsy after hypoxic ischemia in the neonatal brain via inhibition of NKCC1.Journal of neuroinflammation · 2018Article
- Kidney remote ischemic preconditioning as a novel strategy to explore the accurate protective mechanisms underlying remote ischemic preconditioning.Interventional medicine & applied science · 2017Article
- Activation of VEGF/Flk-1-ERK Pathway Induced Blood-Brain Barrier Injury After Microwave Exposure.Molecular neurobiology · 2015Article
- Effect of Glucagon-like Peptide 2 on Tight Junction in Jejunal Epithelium of Weaned Pigs though MAPK Signaling Pathway.Asian-Australasian journal of animal sciences · 2014Article
- High density lipoprotein-associated sphingosine 1-phosphate promotes endothelial barrier function.The Journal of biological chemistry · 2008Article
- Adverse effect of cyclosporin A on barrier functions of cerebral microvascular endothelial cells after hypoxia-reoxygenation damage in vitro.Cellular and molecular neurobiology · 2007Article
- Role of focal adhesion kinase (FAK) in renal ischaemia and reperfusion.Pflugers Archiv : European journal of physiology · 2007Article
- Bile modulates intestinal epithelial barrier function via an extracellular signal related kinase 1/2 dependent mechanism.Intensive care medicine · 2005Article
- Effect of oxidative stress on the junctional proteins of cultured cerebral endothelial cells.Cellular and molecular neurobiology · 2005Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During an ischaemic insult, oedema formation occurs as a consequence of increased vascular permeability. To study mechanisms leading to vascular barrier failure, endothelial cells were exposed to ischaemia (1% O(2) in serum- and glucose-free medium) for 5 h. In in vitro conditions, ischaemia increased paracellular permeability, disassembled actin stress fibres, displaced focal adhesion kinase (FAK) from focal adhesions and enhanced cytoskeletal association of occludin. Reoxygenation restored paracellular barrier function, actin organization and FAK distribution. The mitogen-activated protein kinase (MAPK)/extracellular signal-regulated protein kinase (ERK) was rapidly activated after 30 min, strongly inhibited after 5 h of continuous ischaemia and reactivated 3 times more than control during reoxygenation. Inhibition of ERK activation during reoxygenation with U0126, an inhibitor of the ERK activator, MAPK/ERK kinase 1/2, prevented both barrier restoration and stress-fibre formation, but did not prevent recruitment of FAK to focal contacts. Under normoxic conditions, ERK inhibition led to barrier failure and disassembly of stress fibres only in the absence of serum. These results demonstrate that ERK activity is essential to rebuild a disrupted endothelial barrier after ischaemia and to maintain barrier function in cells exposed to non-ischaemic stress.
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