Vascular Endothelial Growth Factor Localization in the Adult

Maharaj, Arindel S.R.; Saint‐Geniez, Magali; Maldonado, Angel; D'Amore, Patricia A.

doi:10.2353/ajpath.2006.050834

Cited by 258 publications

(242 citation statements)

References 53 publications

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“…Furthermore, recent studies with VEGF antagonists point to a continuing vascular dependence on VEGF in normal adult peripheral capillaries and in the choroid plexus (Baffert et al, 2006;Kamba et al, 2006). In addition to a postulated vessel-stabilizing role for VEGF (Maharaj et al, 2006), vessel stabilization can also be dependent on neurotrophin signaling, as was recently showed in ischemic skeletal muscle (Kermani et al, 2005). The vascular regression observed in the present study, then, may reflect a coordinated reduction in these or other vessel stabilizing molecules.…”

Section: Discussionsupporting

confidence: 78%

Stroke-Evoked Angiogenesis Results in a Transient Population of Microvessels

Friedman

Cheng

et al. 2007

J Cereb Blood Flow Metab

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The role of angiogenesis after stroke is unclear; if angiogenesis supports long-term recovery of blood flow, then microvessel hyperdensity consequent to angiogenesis should persist in infarcted cortex. Here, we assess the long-term stability of ischemia-induced microvessels after 2-h transient rat middle cerebral artery occlusion (tMCAo) followed by 30, 90, or 165 days of reperfusion. Stereological measures of microvessel density were taken adjacent to and within cortical cysts. Vascular permeability was documented by extravasation of immunoglobulin (IgG) and of fluorescein-dextran. After 30 days reperfusion, a significantly increased microvessel volume density (V V ) was restricted to the inner margin of cystic infarcts as compared with the region external to the infarct or contralateral control cortex (F = 42.675, P < 0.001). The hyperdense ischemic vasculature was abnormally leaky to IgG and fluorescein-dextran. Between 30 and 90 days of reperfusion, this vessel hyperdensity regressed significantly and then regressed further but less drastically between 90 and 165 days. Phagocytic macrophages were restricted to the infarct and dynamic changes in their number correlated with microvessel regression. Additional ED-1 labeled inflammatory cells were widely distributed inside and external to the infarct, even after 165 days of reperfusion. These data show that ischemia evoked angiogenesis results, at least in part, in transient populations of leaky microvessels and phagocytic macrophages. This suggests that a major role of this angiogenesis is for the removal of necrotic brain tissue.

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Section: Discussionsupporting

confidence: 78%

Stroke-Evoked Angiogenesis Results in a Transient Population of Microvessels

Friedman

Cheng

et al. 2007

J Cereb Blood Flow Metab

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“…Angiogenesis also requires the activation of VEGF‐VEGFR signalling. Indeed, endothelial cells engaged in angiogenesis express numerous VEGFRs, but they produce only low levels of endogenous VEGF themselves 34. This might be a rational explanation of the finding that VEGF expression alterations are not in accordance with VEGFR‐2 in RF/6A cells.…”

Section: Discussionmentioning

confidence: 99%

Up‐regulated basigin‐2 in microglia induced by hypoxia promotes retinal angiogenesis

Yin

et al. 2017

J Cellular Molecular Medi

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Retinal microglia cells contribute to vascular angiogenesis and vasculopathy induced by relative hypoxia. However, its concrete molecular mechanisms in shaping retinal angiogenesis have not been elucidated. Basigin, being involved in tumour neovasculogenesis, is explored to exert positive effects on retinal angiogenesis induced by microglia. Therefore, we set out to investigate the expression of basigin using a well‐characterized mouse model of oxygen‐induced retinopathy, which recapitulated hypoxia‐induced aberrant neovessel growth. Our results elucidate that basigin is overexpressed in microglia, which accumulating in retinal angiogenic sprouts. In vitro, conditioned media from microglia BV2 under hypoxia treatment increase migration and tube formation of retinal capillary endothelia cells, compared with media from normoxic condition. The angiogenic capacity of BV2 is inhibited after basigin knockdown by small interfering RNAs. A new molecular mechanism for high angiogenic capacity, whereby microglia cells release basigin via up‐regulation of PI3K‐AKT and IGF‐1 pathway to induce angiogenesis is unveiled. Collectively, our results demonstrate that basigin from hypoxic microglia plays a pivotal pro‐angiogenic role, providing new insights into microglia‐promoting retinal angiogenesis.

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“…(Dugel, 2006;Rosenfeld et al, 2006b;Rosenfeld et al, 2005), there is concern about broadly inhibiting VEGF activity in AMD. VEGF is a survival factor for the developing and mature retina (Maharaj et al, 2006). In addition, vision loss can occur from atrophic AMD and geographic atrophy, and patients with neovascular AMD can have geographic atrophy in the same eye (Sunness et al, 1999).…”

Section: Amd Overviewmentioning

confidence: 99%

“…VEGF is important in vascular development (Stone et al, 1995), survival of nascent retinal vessels and in maintaining stable mature vessels (Maharaj et al, 2006). In addition, evidence establishes VEGF signaling as important in the health of the RPE, Bruch's membrane, and choroidal endothelial cells (CECs).…”

Section: Vegf In Outer Retinal Healthmentioning

confidence: 99%

Vascular endothelial growth factor in eye disease

Penn

Madan

Caldwell

et al. 2008

Progress in Retinal and Eye Research

636

527

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Collectively, angiogenic ocular conditions represent the leading cause of irreversible vision loss in developed countries. In the U.S., for example, retinopathy of prematurity, diabetic retinopathy and age-related macular degeneration are the principal causes of blindness in the infant, working age and elderly populations, respectively. Evidence suggests that vascular endothelial growth factor (VEGF), a 40 kDa dimeric glycoprotein, promotes angiogenesis in each of these conditions, making it a highly significant therapeutic target. However, VEGF is pleiotropic, affecting a broad spectrum of endothelial, neuronal and glial behaviors, and confounding the validity of anti-VEGF strategies, particularly under chronic disease conditions. In fact, among other functions VEGF can influence cell proliferation, cell migration, proteolysis, cell survival and vessel permeability in a wide variety of biological contexts. This article will describe the roles played by VEGF in the pathogenesis of retinopathy of prematurity, diabetic retinopathy and age-related macular degeneration. The potential disadvantages of inhibiting VEGF will be discussed, as will the rationales for targeting other VEGF-related modulators of angiogenesis.

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Vascular Endothelial Growth Factor Localization in the Adult

Cited by 258 publications

References 53 publications

Stroke-Evoked Angiogenesis Results in a Transient Population of Microvessels

Stroke-Evoked Angiogenesis Results in a Transient Population of Microvessels

Up‐regulated basigin‐2 in microglia induced by hypoxia promotes retinal angiogenesis

Vascular endothelial growth factor in eye disease

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