Opposing Effects of the Angiopoietins on the Thrombin-Induced Permeability of Human Pulmonary Microvascular Endothelial Cells 英文参考文献.docVIP

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Opposing Effects of the Angiopoietins on the Thrombin-Induced Permeability of Human Pulmonary Microvascular Endothelial Cells 英文参考文献.doc

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Opposing Effects of the Angiopoietins on the Thrombin-Induced Permeability of Human Pulmonary Microvascular Endothelial Cells 英文参考文献

OpposingEffectsoftheAngiopoietinsontheThrombin- InducedPermeabilityofHumanPulmonary MicrovascularEndothelialCells MelanievanderHeijden1,2,GeertenP.vanNieuwAmerongen2*,JanvanBezu2,MarinusA.Paul3,A.B. JohanGroeneveld1,VictorW.M.vanHinsbergh2 1DepartmentofIntensiveCare,InstituteforCardiovascularResearch,VUUniversityMedicalCentre,Amsterdam,TheNetherlands,2DepartmentofPhysiology,Institute for Cardiovascular Research, VU University Medical Centre, Amsterdam, The Netherlands, 3Department of Cardiothoracic Surgery, VU University Medical Centre, Amsterdam,TheNetherlands Abstract Background:Angiopoietin-2(Ang-2)isassociatedwithlunginjuryinALI/ARDS.Asendothelialactivationbythrombinplays aroleinthepermeabilityofacutelunginjuryandAng-2maymodulatethekineticsofthrombin-inducedpermeabilityby impairing the organization of vascular endothelial (VE-)cadherin, and affecting small Rho GTPases in human pulmonary microvascular endothelial cells (HPMVECs), we hypothesized that Ang-2 acts as a sensitizer of thrombin-induced hyperpermeabilityofHPMVECs,opposedbyAng-1. Methodology/Principal Findings: Permeability was assessed by measuring macromoleculepassage andtransendothelial electricalresistance(TEER).Angiopoietinsdidnotaffectbasalpermeability.Nevertheless,theyhadopposingeffectsonthe thrombin-inducedpermeability,inparticularintheinitialphase.Ang-2enhancedtheinitialpermeabilityincrease(passage, P=0.010; TEER, P=0.021) in parallel with impairment of VE-cadherin organization without affecting VE-cadherin Tyr685 phosphorylation or increasing RhoA activity. Ang-2 also increased intercellular gap formation. Ang-1 preincubation increased Rac1 activity, enforced the VE-cadherin organization, reduced the initial thrombin-induced permeability (TEER, P=0.027), while Rac1 activity simultaneously normalized, and reduced RhoA activity at 15min thrombin exposure (P=0.039),butnotatearliertimepoints.ThesimultaneouspresenceofAng-2largelypreventedtheeffectofAng-1onTEER andmacromoleculepassage. Conclusions