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eNOS-induced vascul...
eNOS-induced vascular barrier disruption in retinopathy by c-Src activation and tyrosine phosphorylation of VE-cadherin
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- Ninchoji, Takeshi (författare)
- Uppsala universitet,Vaskulärbiologi
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- Love, Dominic T. (författare)
- Uppsala universitet,Vaskulärbiologi
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- Smith, Ross O. (författare)
- Uppsala universitet,Vaskulärbiologi
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- Hedlund, Marie (författare)
- Uppsala universitet,Vaskulärbiologi
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- Vestweber, Dietmar (författare)
- Max Planck Inst Mol Biomed, Münster, Germany
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- Sessa, William C. (författare)
- Yale Univ, Sch Med, Dept Pharmacol, New Haven, CT 06510 USA.;Yale Univ, Sch Med, Vasc Biol & Therapeut Program, New Haven, CT 06510 USA
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- Claesson-Welsh, Lena (författare)
- Uppsala universitet,Vaskulärbiologi
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(creator_code:org_t)
- eLife Sciences Publications Ltd, 2021
- 2021
- Engelska.
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Ingår i: eLIFE. - : eLife Sciences Publications Ltd. - 2050-084X. ; 10
- Relaterad länk:
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https://doi.org/10.7...
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https://uu.diva-port... (primary) (Raw object)
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https://urn.kb.se/re...
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https://doi.org/10.7...
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Abstract
Ämnesord
Stäng
- Background:Hypoxia and consequent production of vascular endothelial growth factor A (VEGFA) promote blood vessel leakiness and edema in ocular diseases. Anti-VEGFA therapeutics may aggravate hypoxia; therefore, therapy development is needed.Methods:Oxygen-induced retinopathy was used as a model to test the role of nitric oxide (NO) in pathological neovascularization and vessel permeability. Suppression of NO formation was achieved chemically using L-NMMA, or genetically, in endothelial NO synthase serine to alanine (S1176A) mutant mice.Results:Suppression of NO formation resulted in reduced retinal neoangiogenesis. Remaining vascular tufts exhibited reduced vascular leakage through stabilized endothelial adherens junctions, manifested as reduced phosphorylation of vascular endothelial (VE)-cadherin Y685 in a c-Src-dependent manner. Treatment with a single dose of L-NMMA in established retinopathy restored the vascular barrier and prevented leakage.Conclusions:We conclude that NO destabilizes adheren junctions, resulting in vascular hyperpermeability, by converging with the VEGFA/VEGFR2/c-Src/VE-cadherin pathway.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Cell- och molekylärbiologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Cell and Molecular Biology (hsv//eng)
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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