About: VEGF isoforms have differential effects on permeability of human pulmonary microvascular endothelial cells

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An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	VEGF isoforms have differential effects on permeability of human pulmonary microvascular endothelial cells
Creator	Barratt, Shaney Blythe, Thomas Jarrett, Caroline Millar, Ann Ourradi, Khadija Welsh, Gavin
source	PMC
abstract	BACKGROUND: Alternative splicing of Vascular endothelial growth factor-A mRNA transcripts (commonly referred as VEGF) leads to the generation of functionally differing isoforms, the relative amounts of which have potentially significant physiological outcomes in conditions such as acute respiratory distress syndrome (ARDS). The effect of such isoforms on pulmonary vascular permeability is unknown. We hypothesised that VEGF(165)a and VEGF(165)b isoforms would have differing effects on pulmonary vascular permeability caused by differential activation of intercellular signal transduction pathways. METHOD: To test this hypothesis we investigated the physiological effect of VEGF(165)a and VEGF(165)b on Human Pulmonary Microvascular Endothelial Cell (HPMEC) permeability using three different methods: trans-endothelial electrical resistance (TEER), Electric cell-substrate impedance sensing (ECIS) and FITC-BSA passage. In addition, potential downstream signalling pathways of the VEGF isoforms were investigated by Western blotting and the use of specific signalling inhibitors. RESULTS: VEGF(165)a increased HPMEC permeability using all three methods (paracellular and transcellular) and led to associated VE-cadherin and actin stress fibre changes. In contrast, VEGF(165)b decreased paracellular permeability and did not induce changes in VE-cadherin cell distribution. Furthermore, VEGF(165)a and VEGF(165)b had differing effects on both the phosphorylation of VEGF receptors and downstream signalling proteins pMEK, p42/44MAPK, p38 MAPK, pAKT and peNOS. Interestingly specific inhibition of the pMEK, p38 MAPK, PI3 kinase and eNOS pathways blocked the effects of both VEGF(165)a and VEGF(165)b on paracellular permeability and the effect of VEGF(165)a on proliferation/migration, suggesting that this difference in cellular response is mediated by an as yet unidentified signalling pathway(s). CONCLUSION: This study demonstrates that the novel isoform VEGF(165)a and VEGF(165)b induce differing effects on permeability in pulmonary microvascular endothelial cells.
has issue date	2017-06-02(xsd:dateTime)
bibo:doi	10.1186/s12931-017-0602-1
bibo:pmid	28578669
has license	cc-by
sha1sum (hex)	d9b6a333c49c59ef249831dc4c062aee5a9d7683
schema:url	https://doi.org/10.1186/s12931-017-0602-1
resource representing a document's title	VEGF isoforms have differential effects on permeability of human pulmonary microvascular endothelial cells
has PubMed Central identifier	PMC5457598
has PubMed identifier	28578669
schema:publication	Respir Res
resource representing a document's body	covid:d9b6a333c49c59ef249831dc4c062aee5a9d7683#body_text
is schema:about of	named entity 'proliferation' named entity 'VEGF receptors' named entity 'The' named entity 'VE-cadherin' named entity 'phosphorylation' named entity 'cellular' named entity 'acute respiratory distress syndrome (ARDS)' named entity 'paracellular' named entity 'signal transduction pathways' named entity 'response' named entity 'investigated' named entity 'stress fibre' named entity 'VEGF' named entity 'relative' named entity 'endothelial' named entity 'VEGF' named entity 'physiological' named entity 'VEGF' named entity 'VEGF' named entity 'VEGF' named entity 'isoforms' named entity 'stress fibre' named entity 'isoforms' named entity 'pulmonary vascular' named entity 'kinase' named entity 'VE-cadherin' named entity 'permeability' named entity 'actin' named entity 'VEGF' named entity 'Electric cell-substrate impedance sensing' named entity 'signalling pathway' named entity 'endothelial cells' named entity 'VEGF' named entity 'phosphorylation' named entity 'permeability' named entity 'VEGF' named entity 'bioactivity' named entity 'AKT' named entity 'monolayer' named entity 'VEGF' named entity 'AKT' named entity 'VEGF' named entity 'VEGF' named entity 'VEGF' named entity 'FITC' named entity 'endothelial cells' named entity 'paracellular permeability' named entity 'VEGF' named entity 'LY294002' named entity 'compartmentalisation' named entity 'tyr' named entity 'p38' named entity 'in-vitro' named entity 'permeability' named entity '19, 20' named entity 'isoforms' named entity 'VEGF' named entity 'VEGF' named entity 'loading control' named entity 'VEGF' named entity 'VEGF' named entity 'VEGF' named entity 'phosphorylation' named entity 'permeability' named entity 'monolayer' named entity 'VEGF' named entity 'cell permeability' named entity 'phosphorylation' named entity 'paracellularly' named entity 'systemic circulation' named entity 'HUVEC' named entity 'VEGF' named entity 'basal medium' named entity 'p38MAPK' named entity 'phosphatidylinositol' named entity 'VEGF'

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