['The pro-inflammatory cytokine, tumor necrosis factor-α (TNF-α), is expressed in ischemic tissue and is known to modulate angiogenesis; however, the role of the two distinct TNF-α receptors, TNFR1 and TNFR2, in mediating angiogenic signaling after cerebral ischemic stroke is relatively unknown.', 'C57BL6 mice were subject to 90\xa0min of ischemia by temporary occlusion of the middle cerebral artery (MCAO) and given daily intra-cerebroventricular injections of antibodies against TNFR1, TNFR2 or control IgG (doses of 10, 50, and 100\xa0ng/day) for 4\xa0days following 90\xa0min MCAO. Vascular remodeling and α5β1 and αVβ3 integrin expression were then examined in the brains of these mice after 4, 7, and 14\xa0days post-ischemia. In parallel in vitro studies, flow cytometry was used to determine the influence of TNF-α on proliferation and integrin expression of human brain microvascular endothelial cells (HBMECs).', 'The post-ischemic cerebral angiogenic response was inhibited by antibodies against TNFR1 but not TNFR2, and this correlated with reduced endothelial proliferation and decreased α5β1 and αVβ3 integrin expression after 4 and 7\xa0days post-ischemia. Consistent with these findings, in vitro studies showed that TNF-α induced endothelial proliferation and upregulation of α5β1 and αVβ3 integrins was abrogated by anti-TNFR1 but not anti-TNFR2 antibodies in cultured HBMECs. In addition, blocking antibodies to α5β1 and αVβ3 integrins significantly inhibited TNF-α-induced HBMEC proliferation.'] Is cerebral ischemia-induced angiogenesis dependent on tumor necrosis factor receptor 1-mediated upregulation of α5β1 and αVβ3 integrins?