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1、HEMOSTASIS,THROMBOSIS,ANDVASCULARBIOLOGYTrackingangiogenesisinducedbyskinwoundingandcontacthypersensitivityusingaVegfr2-luciferasetransgenicmouseNingZhang,ZuxuFang,PamelaR.Contag,AnthonyF.Purchio,andDavidB.WestThevascularendothelialgrowthfactor-2latedwithendogenousVEGFR2mRNAmentwithoxa
2、zolone,Vegfr2-lucexpres-(VEGFR2)geneistranscriptionallyregu-expression.Inacutaneouswound-sionwasinducedintheear.Treatmentbylatedduringangiogenesis.Theabilitytohealingmodel,Vegfr2-lucexpressionwasdexamethasonemarkedlysuppressedmonitorandquantifyVEGFR2expressioninducedinthewoundtissue.Hi
3、stologicVegfr2-lucexpressionandleukocyteinfil-invivomayfacilitateabetterunderstand-andimmunohistochemicalstudiestrationintheearandwascorrelatedwithingoftheroleofVEGFR2indifferentshowedsignificantmacrophageinfiltra-reduceddermaledemaandepidermalhy-states.Herewedescribeatransgenictionintoth
4、ewoundandinductionofperplasia.TheVegfr2-lucmodelwillbevalu-mouse,Vegfr2-luc,inwhichaluciferaseVegfr2-lucexpressioninendothelialandableinmonitoringtheabilityofdrugstoreporterisundercontrolofthemurinestromalcells.Dexamethasonesignifi-affectangiogenesisinvivo.(Blood.2004;VEGFR2promoter.Ina
5、dultmice,lucif-cantlysuppressedVegfr2-lucexpression103:617-626)eraseactivitywashighestinlungandandmacrophageinfiltrationintotheuterus,intermediateinheart,skin,andwound,resultingindelayedhealingandkidney,andlowerinothertissues.Lucif-impairedangiogenesis.Inaskinhyper-eraseexpressioninthes
6、etissuescorre-sensitivityreactionproducedbytreat-©2004byTheAmericanSocietyofHematologyIntroductionAngiogenesisistheprocessofcapillarysproutingfrompre-thy,9rheumatoidarthritis,10psoriasis,11andhypersensitivityexistingbloodvessels.1Theangiogenesisprocessischaracterizedskinreactions.12,13
7、byvasodilation,increasedplasmaleakage,remodelingoftheAngiogenesisisanimportantpartofwoundhealing,1whichextracellularmatrix,up-regulationofgrowthfactorreceptors,involvestheinductionofproinflammatorycytokinesandvariousproliferationanddifferentiationofendothelialcells,andrecruit-growthfa
