Inhibition of endogenous VEGF impedes revascularization and astroglial proliferation: roles for VEGF in brain repair

Krum, Janette M.; Khaibullina, Alfia

doi:10.1016/s0014-4886(03)00039-6

Cited by 134 publications

(90 citation statements)

References 75 publications

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“…On the other hand, VEGF-A could be used to treat neurodegenerative and neuropathic conditions by simultaneously enhancing blood vessel growth, neurogenesis and neuroprotection, provided that we learn to control its potential negative effects. Most importantly, VEGF-A can increase vascular permeability and thereby disrupt the blood-brain barrier and promote inflammatory cell infiltration (Kalaria et al, 1998;Krum and Khaibullina, 2003;Krum et al, 2002;Proescholdt et al, 1999;Zhang et al, 2000). Defining the role of VEGF-A and its receptors in neurodevelopment and in adult neural homeostasis and pathology is therefore a priority for the future.…”

Section: Discussionmentioning

confidence: 99%

Diverse roles for VEGF-A in the nervous system

2012

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Vascular endothelial growth factor A (VEGF-A) is best known for its essential roles in blood vessel growth. However, evidence has emerged that VEGF-A also promotes a wide range of neuronal functions, both in vitro and in vivo, including neurogenesis, neuronal migration, neuronal survival and axon guidance. Recent studies have employed mouse models to distinguish the direct effects of VEGF on neurons from its indirect, vessel-mediated effects. Ultimately, refining our knowledge of VEGF signalling pathways in neurons should help us to understand how the current use of therapeutics targeting the VEGF pathway in cancer and eye disease might be expanded to promote neuronal health and nerve repair.

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Section: Discussionmentioning

confidence: 99%

Diverse roles for VEGF-A in the nervous system

2012

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“…15 To this end, there is substantial evidence demonstrating the importance of VEGF in brain tissue repair and in CNS wound healing. [45][46][47] Exogenous administration of VEGF to injured brain tissue improved wound repair, functional response, and decreased apoptosis in rats. 48 Increased levels of VEGF are often detected in tissues and biologic samples from malaria patients.…”

Section: Vegf and Brain: Neuroprotection And Neurodegenerationmentioning

confidence: 99%

Protective or pathogenic effects of vascular endothelial growth factor (VEGF) as potential biomarker in cerebral malaria

Canavese

Spaccapelo

2014

Pathogens and Global Health

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Cerebral malaria (CM) is the major lethal complication of Plasmodium falciparum infection. It is characterized by persistent coma along with symmetrical motor signs. Several clinical, histopathological, and laboratory studies have suggested that cytoadherence of parasitized erythrocytes, neural injury by malarial toxin, and excessive inflammatory cytokine production are possible pathogenic mechanisms. Although the detailed pathophysiology of CM remains unsolved, it is thought that the binding of parasitized erythrocytes to the cerebral endothelia of microvessels, leading to their occlusion and the consequent angiogenic dysregulation play a key role in the disease pathogenesis. Recent evidences showed that vascular endothelial growth factor (VEGF) and its receptor-related molecules are over-expressed in the brain tissues of CM patients, as well as increased levels of VEGF are detectable in biologic samples from malaria patients. Whether the modulation of VEGF is causative agent of CM mortality or a specific phenotype of patients with susceptibility to fatal CM needs further evaluation. Currently, there is no biological test available to confirm the diagnosis of CM and its complications. It is hoped that development of biomarkers to identify patients and potential risk for adverse outcomes would greatly enhance better intervention and clinical management to improve the outcomes. We review and discuss here what it is currently known in regard to the role of VEGF in CM as well as VEGF as a potential biomarker.

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“…Some authors have shown that the infusion of VEGF induces an astroglial response after the injury, that is lowered by blocking endogenous VEGF (Krum et al, 2002;Krum and Khaibullina, 2003;Mani et al, 2005). These results have also been reproduced in vitro (Rosenstein et al, 2003;Mani et al, 2005).…”

Section: Astroglial Reactionmentioning

confidence: 81%

“…Some authors have studied the post-traumatic effects of VEGF administration and inhibition in adults, where scarce endogenous VEGF secretion remains (Krum et al, 2002;Krum and Khaibullina, 2003). Among the observed effects, the inhibition of VEGF receptor 2 increases lesion area and cellular death (Skold et al, 2006).…”

Section: Introductionmentioning

confidence: 99%