@entity519 -induced @entity1611 governs both physiological @entity8038 and pathological @entity2479 . In the current paper, the mechanisms of physiological and @entity16110 are compared and contrasted. During @entity16110 , both the absolute and relative expression levels for VEGF164 increased to a greater degree than during physiological neovascularization. Furthermore, extensive leukocyte adhesion was observed at the leading edge of pathological, but not physiological, neovascularization. When a VEGF164-specific neutralizing aptamer was administered, it potently suppressed the leukocyte adhesion and @entity16110 , whereas it had little or no effect on physiological neovascularization. In parallel experiments, genetically altered VEGF164-deficient (VEGF120/188) @entity19 exhibited no difference in physiological neovascularization when compared with wild-type ( @entity1611 +/+) controls. In contrast, administration of a @entity9842 /Fc fusion protein, which blocks all @entity1611 isoforms, led to significant suppression of both pathological and physiological neovascularization. In addition, the targeted inactivation of monocyte lineage cells with @entity19160 -liposomes led to the suppression of @entity16110 . Conversely, the blockade of T lymphocyte-mediated immune responses with an anti- @entity19649 antibody exacerbated @entity16110 . These data highlight important molecular and cellular differences between physiological and pathological @entity2479 . During @entity16110 , VEGF164 selectively induces @entity32 and cellular immunity. These processes provide positive and negative angiogenic regulation, respectively. Together, new therapeutic approaches for selectively targeting pathological, but not physiological, @entity2479 are outlined.

VEGF164-mediated XXXX is required for pathological, but not physiological, ischemia-induced @entity2479 .

@entity32 :: ('MESH:D007249', 'Disease') :: ['inflammation'] @entity9842 :: ('14254(Tax:10090)', 'Gene') :: ['VEGFR-1'] @entity2479 :: ('MESH:D012173', 'Disease') :: ['retinal neovascularization'] @entity19 :: ('10090', 'Species') :: ['mice'] @entity8038 :: ('MESH:D058456', 'Disease') :: ['retinal vascular development'] @entity519 :: ('MESH:D000860', 'Disease') :: ['Hypoxia'] @entity19649 :: ('12481(Tax:10090)', 'Gene') :: ['CD2'] @entity1611 :: ('22339(Tax:10090)', 'Gene') :: ['VEGF'] @entity19160 :: ('MESH:D004002', 'Chemical') :: ['clodronate'] @entity16110 :: ('MESH:D009389', 'Disease') :: ['pathological neovascularization']
@entity32 :: (MESH:D007249,Disease) :: ['inflammation']
