 stimulate the expression of angiogenic integrins, thereby activating the integrin signaling pathway and promoting endothelial cell adhesion and migration. Specific Aim 2: To determine whether ROS elevate angiogenesis through triggering of endothelial cell proliferation and tube formation in the infarcted heart. Our hypothesis is that ROS activate the expressions of vascular endothelial growth factor (VEGF)
stimulate the expression of angiogenic integrins, thereby activating the integrin signaling pathway and advertise endothelial cellular telephone adhesion and migration. Specific Aim 2: To determine whether ROS lift angiogenesis through trigger of endothelial cell proliferation and tube geological formation in the infarcted kernel. Our hypothesis is that ROS activate the expressions of vascular endothelial growth gene (VEGF )
 stlmulate the expression on angiogenic intggeins, tiereby zctivativg the integrin signaling pavhwat and promoting endothelial cell adhvsion and migcation. Specific Ejm 2: To determjke whztier ROS elevate angiogenevis through trhgeexing of endothelial cell proliferatijn and yuhe formation ig tht igfardneb heart. Our hypothesis is that DOS actpvate the expressoons of vascular endotheliwl ggowth factor (VEGF)
stimulate the expression of angiogenic integrins, thereby integrin pathway and endothelial cell adhesion To whether ROS elevate through triggering of cell proliferation and tube formation in infarcted heart. Our hypothesis is that ROS activate the expressions of vascular endothelial factor (VEGF)
 stimulate the expression of aNgiogenic iNtegrIns, TheReBy acTivaTing the integriN SignAling pathway and promotiNg endOtHEliaL CeLl adhEsion anD MiGRAtiOn. spEciFiC aiM 2: To deTerMine wheTher ROS eleVatE aNgiogenesis tHRoUgh triggerIng Of endotheliaL ceLl prolIfEraTIon anD tuBe forMation IN the inFarcted heArT. our hypOThesis iS THaT ROS Activate the expresSIoNS of vascular endOtheliAl GRoWTH faCtoR (VEGF)
 stimulate the expressionof angioge nic i nte gri ns , th ereb y activating t h e in tegrin signaling pathw ay an dp romo t in g end othelia l  c e l l a dh es ion  a n dmigra tio n. Spec ific Aim 2 : T odetermine wh e th er ROS ele vat e angiogenes isthroug htri g gerin g o f end otheli a l cell  prolifer at i on and tube fo r m at ionin the infarctedh ea r t. Our hypothe sis is  t h at R OSact ivate theex press i ons ofv as c u l are ndothelial gr owth factor (VE GF)
 stimulate_the expression_of angiogenic integrins, thereby_activating the_integrin_signaling pathway_and_promoting endothelial cell_adhesion and migration._Specific Aim 2: To_determine whether ROS_elevate_angiogenesis through triggering of endothelial cell proliferation and tube formation in the infarcted heart._Our_hypothesis is_that_ROS_activate the expressions of vascular_endothelial growth factor (VEGF)