Vascular Endothelial Growth Factor Expression, Vascular Volume, and Capillary Permeability in Human Brain Tumors

Machein, Márcia Regina; Kullmer, Johannes; Fiebich, Bernd L.; Plate, Karl H.; Warnke, Peter C.

doi:10.1097/00006123-199904000-00022

Cited by 100 publications

(48 citation statements)

References 25 publications

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“…This is probably due to the presence of vascular endothelial growth factor (VEGF) secreted by astrocytomas. VEGF increases the proliferation of ECs resulting in a sufficient vascularization and BBB function of the tumor blood vessels (Machein et al, 1999).…”

Section: Pathology Of the Bbb-role Of Glia Cellsmentioning

confidence: 99%

“…Apparently, glioma or astrocytoma cells lack distinct signals necessary to maintain the BBB in cerebral ECs. Excessive VEGF production could overstimulate EC proliferation and simultaneously suppress the establishment of BBB properties in EC (Machein et al, 1999). Capillaries of advanced tumors show abnormalities too; besides the lack of BBB-related characteristics a different composition of the basement membrane (e.g., increased levels of tenascin) has been observed (Rascher et al, 2002).…”

Section: Pathology Of the Bbb-role Of Glia Cellsmentioning

confidence: 99%

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In Search of the Astrocytic Factor(s) Modulating Blood–Brain Barrier Functions in Brain Capillary Endothelial Cells In Vitro

2005

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(1) The blood-brain barrier (BBB) is formed by brain capillary endothelial cells (ECs). There are various cell types, in particular astrocytes, but also pericytes and neurons, located in close vicinity to the capillary ECs which may influence formation and function of the BBB. Based on this consideration, this paper discusses various aspects of the influence of the surrounding cells on brain capillary ECs with special focus on the role of astrocytes. (2) Based on the morphology of the BBB, important aspects of brain EC functions are summarized, such as transport functions and maintenance of low paracellular permeability. Moreover, various facets are discussed with respect to the influence of astrocytes, pericytes, microglia, and neurons on the BBB. Data on the role of glial cells in the ontogenesis of the BBB are presented subsequently. The knowledge on this subject is far from being complete, however, these data imply that the neural/neuronal environment rather than glial cells may be of importance in the maturation of the barrier. (3) The role of glial cells in the induction and maintenance of the BBB is discussed under physiological as well as pathological conditions. Although the literature presents manifold evidence for a great variety of effects induced by astroglia, there are also many controversies, which may result from different cellular models and experimental conditions used in the respective studies. Numerous factors secreted by astrocytes have been shown to induce a BBB phenotype. On the molecular level, increased expression of barrier-relevant proteins (e.g., tight junction proteins) is documented in the presence of astrocyte-derived factors, and many studies demonstrate the improvement of physiological parameters, such as increased transendothelial resistance and decreased paracellular permeability, in different in vitro models of the BBB. Moreover, one has to take into account that the interaction of brain ECs and astrocytes is bi-directional, and that the other cell types surrounding the brain microvasculature also contribute to BBB function or dysfunction, respectively. (4) In conclusion, it is expected that the present and future research focused on molecular mechanisms and signaling pathways will produce new and exciting insights into the complex network of BBB regulation: the cornerstone is laid.

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Section: Pathology Of the Bbb-role Of Glia Cellsmentioning

confidence: 99%

Section: Pathology Of the Bbb-role Of Glia Cellsmentioning

confidence: 99%

In Search of the Astrocytic Factor(s) Modulating Blood–Brain Barrier Functions in Brain Capillary Endothelial Cells In Vitro

2005

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“…In rats, VEGF expression in the brain is strongly up-regulated by alveolar hypoxia; based on this ®nding, a role of VEGF in the pathogenesis of HACE has been suggested (Xu and Severinghaus 1998). In humans, VEGF augments vascular permeability in brain tumors (Machein et al 1999). Interestingly, corticosteroids inhibit the expression of VEGF in human vascular smooth muscle cells in vitro (Nauck et al 1998), and improve symptoms of AMS in vivo (Ward et al 1995).…”

Section: Introductionmentioning

confidence: 99%

Effects of high-altitude exposure on vascular endothelial growth factor levels in man

Walter

Maggiorini

Scherrer

et al. 2001

European Journal of Applied Physiology

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Vascular endothelial growth factor (VEGF) is an endothelial cell mitogen and permeability factor that is inducible by hypoxia. Its contribution to high-altitude illness in man is unknown. We measured VEGF levels in 14 mountaineers at low altitude (490 m) and 24 h after their arrival at high altitude (4,559 m). At high altitude, VEGF increased from [mean (SEM)] 32.5 (9.2) to 60.9 (18.5) pg.ml(-1) (P < 0.004) in the arterial blood, and from 15.9 (2.9) to 49.3 (15.9) pg.ml(-1) (P= 0.0001) in the mixed venous blood. Whereas at low altitude venous and arterial VEGF levels were not statistically different from each other (P= 0.065), the VEGF concentration was significantly lower in venous than in arterial blood samples at high altitude (P=0.004). The pulmonary capillary VEGF concentration remained unchanged at high altitude [14.8 (2.5) vs 17.1 (5.4) pg.ml(-1), P=0.85]. VEGF levels in the nine mountaineers who developed symptoms of acute mountain sickness (AMS), and in the six subjects who had radiographic evidence of high-altitude pulmonary edema were similar to those in subjects without symptoms. VEGF was not correlated with either AMS scores, mean pulmonary arterial pressures, arterial partial pressure of O2, or alveolar-arterial O2 gradients. We conclude that VEGF release is stimulated at high altitude, but that VEGF is probably not related to high-altitude illness.

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“…Previous studies have documented expression of VEGF (Chan et al, 1998;Machein et al, 1999;Schmidt et al, 1999) and PGF in human primary brain tumors (Nomura et al, 1998). This study con rmed the presence of low amounts of PGF in human astrocytomas by PCR experiments, but not by Northern blot experiments.…”

Section: Discussionmentioning

confidence: 98%

Expression of vascular endothelial growth factor-b in human astrocytoma

Gollmer¹,

Ladoux²,

Gioanni³

et al. 2000

Neuro-Oncol

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Vascular Endothelial Growth Factor Expression, Vascular Volume, and Capillary Permeability in Human Brain Tumors

Cited by 100 publications

References 25 publications

In Search of the Astrocytic Factor(s) Modulating Blood–Brain Barrier Functions in Brain Capillary Endothelial Cells In Vitro

In Search of the Astrocytic Factor(s) Modulating Blood–Brain Barrier Functions in Brain Capillary Endothelial Cells In Vitro

Effects of high-altitude exposure on vascular endothelial growth factor levels in man

Expression of vascular endothelial growth factor-b in human astrocytoma

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