Effects of Vascular Permeability Factor on the Permeability of Cultured Endothelial Cells from Brain Capillaries

Zhao, Limin; Zhang, Miao Miao; Ng, Ka‐Yun

doi:10.1097/00005344-199807000-00001

Cited by 28 publications

(10 citation statements)

References 15 publications

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“…Furthermore, intravenous administration of rhVEGF 165 did not increase BBB leakage in nonischemic rats. These findings are consistent with and extend previous studies (57)(58)(59)(60). Intracarotid infusion of VEGF to nonischemic rats did not increase extravasation of FITC and 125 I-BSA from normal brain microvessels (59).…”

Section: Discussionsupporting

confidence: 93%

“…These data indicate that the receptors for VEGF are located on the abluminal side of vessels (58,60,61). However, our findings extend previous observations by demonstrating that intravenous administration of VEGF increases BBB leakage only in the ischemic lesion.…”

Section: Figurementioning

confidence: 90%

“…increased permeability of cultured brain microvessel endothelial cells (58,60,61). These data indicate that the receptors for VEGF are located on the abluminal side of vessels (58,60,61).…”

Section: Figurementioning

confidence: 99%

See 2 more Smart Citations

VEGF enhances angiogenesis and promotes blood-brain barrier leakage in the ischemic brain

Zhang

Zhang²,

Jiang³

et al. 2000

J. Clin. Invest.

1,181

944

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Section: Discussionsupporting

confidence: 93%

Section: Figurementioning

confidence: 90%

See 1 more Smart Citation

VEGF enhances angiogenesis and promotes blood-brain barrier leakage in the ischemic brain

Zhang

Zhang²,

Jiang³

et al. 2000

J. Clin. Invest.

1,181

944

View full text Add to dashboard Cite

“…In the current study, we reveal a potential non-invasive therapeutic approach for enhancement of BBB permeability to facilitate CNS drug delivery, systemic pre-injection of VEGF. This result is consistent with an in vitro study showing that VEGF dose-dependently and reversibly enhanced permeability through cultured endothelial cell layers [30]. In contrast, others have reported that systemic application of VEGF only increases the permeability of already compromised BBA.…”

Section: Discussionsupporting

confidence: 92%

Vascular Endothelial Growth Factors Enhance the Permeability of the Mouse Blood-brain Barrier

et al. 2014

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The blood-brain barrier (BBB) impedes entry of many drugs into the brain, limiting clinical efficacy. A safe and efficient method for reversibly increasing BBB permeability would greatly facilitate central nervous system (CNS) drug delivery and expand the range of possible therapeutics to include water soluble compounds, proteins, nucleotides, and other large molecules. We examined the effect of vascular endothelial growth factor (VEGF) on BBB permeability in Kunming (KM) mice. Human VEGF165 was administered to treatment groups at two concentrations (1.6 or 3.0 µg/mouse), while controls received equal-volume saline. Changes in BBB permeability were measured by parenchymal accumulation of the contrast agent Gd-DTPA as assessed by 7 T magnetic resonance imaging (MRI). Mice were then injected with Evans blue, sacrificed 0.5 h later, and perfused transcardially. Brains were removed, fixed, and sectioned for histological study. Both VEGF groups exhibited a significantly greater signal intensity from the cerebral cortex and basal ganglia than controls (P<0.001). Evans blue fluorescence intensity was higher in the parenchyma and lower in the cerebrovasculature of VEGF-treated animals compared to controls. No significant brain edema was observed by diffusion weighted MRI (DWI) or histological staining. Exogenous application of VEGF can increase the permeability of the BBB without causing brain edema. Pretreatment with VEGF may be a feasible method to facilitate drug delivery into the CNS.

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“…Nevertheless, one possible role that the changes in circulating levels of VEGF may play is related to its enhancing influence on the expression of glucose transporter (GLUT)1 at the blood-brain barrier (BBB) (28,45). Furthermore, VEGF mediates induction of endothelial fenestrations (4), thereby increasing transport of small molecules such as sucrose and fluorescein across the BBB (48,50). Through these actions at the BBB, a decrease in VEGF as seen here after acute hypoxia could diminish glucose transfer across the BBB that eventually may be neuroprotective.…”

Section: Discussionmentioning

confidence: 96%

Acute hypoxia decreases plasma VEGF concentration in healthy humans

Oltmanns

Gehring

Rudolf

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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Vascular endothelial growth factor (VEGF) is known to be upregulated by hypoxia in vitro. However, in vivo data about VEGF regulation in chronic hypoxic diseases are conflicting. We investigated the effects of hypoxia on plasma VEGF concentration in healthy subjects. To control known confounders, such as insulin, glucose concentrations, or exercise, hypoxic effects on VEGF were studied during experimentally clamping glucose concentrations at rest. In a double-blind crossover study design, we induced hypoxia for 30 min by decreasing oxygen saturation to 75% (vs. normoxic control) in 14 healthy men. Plasma VEGF concentration was determined at baseline, immediately after hypoxia had ended, and after a further 150 min. Levels of its soluble (s)Flt-1 receptor were assessed at baseline and at the end of the clamp. In parallel, catecholamine and cortisol levels were monitored. To investigate potential effects of glucose administration on the release of VEGF, we performed a third session, reducing glucose infusion for 30 min while serum insulin was held stable thereby inducing hypoglycemia. Hypoxia decreased VEGF levels compared with the normoxic control ( P < 0.05). VEGF concentrations increased during hypoglycemia ( P < 0.02) but were comparable to the normoglycemic control at the end of the clamp ( P > 0.80). sFlt-1 receptor concentration remained unchanged during hypoxia and hypoglycemia compared with control (both P > 0.4). Epinephrine concentration ( P < 0.01) increased upon hypoxia, whereas norepinephrine and cortisol did not change. Contrary to in vitro studies, in healthy humans hypoxia decreases plasma VEGF concentration, suggesting that systemic VEGF concentration may be differently regulated than the expression on cellular basis.

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Effects of Vascular Permeability Factor on the Permeability of Cultured Endothelial Cells from Brain Capillaries

Cited by 28 publications

References 15 publications

VEGF enhances angiogenesis and promotes blood-brain barrier leakage in the ischemic brain

VEGF enhances angiogenesis and promotes blood-brain barrier leakage in the ischemic brain

Vascular Endothelial Growth Factors Enhance the Permeability of the Mouse Blood-brain Barrier

Acute hypoxia decreases plasma VEGF concentration in healthy humans

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