Possible Relationship between Vascular Permeability Factors, Endothelial Cells, and Peritumoral Brain Edema

Criscuolo, Gregory R.

doi:10.1007/978-1-4899-0721-9_28

Cited by 4 publications

(4 citation statements)

References 86 publications

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“…A variety of cultured endothelial cells has been shown to undergo a rapid (Ͻ 60 second) and reversible induction of cytosolic calcium following VPF stimulation. 9 There also appears to be a rapid induction of inositol 1,4,5 triphosphate, suggesting that a second messenger involving inositol lipid hydrolysis may be involved. 17 As indicated in this discussion, VEG/PFs have been isolated from a variety of tumors.…”

Section: Discussionmentioning

confidence: 98%

“…Several studies have attested to VEG/PF's heparinbinding affinity, which proved instrumental in its early purification. 9,39 It has been hypothesized that this heparin affinity is of physiological import, because the glycocalyx of vascular endothelial cells expresses abundant heparinlike moieties. Moreover, it was shown that coinjection of VPF with heparinase inhibited VPF activity in the Miles assay.…”

Section: Discussionmentioning

confidence: 99%

“…In vitro studies examining VEG/PFinduced calcium transients in endothelial cells support this alternative hypothesis. 9…”

Section: Discussionmentioning

confidence: 99%

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Vascular endothelial growth/permeability factor expression in human glioma specimens: correlation with vasogenic brain edema and tumor-associated cysts

Strugar¹,

Criscuolo²,

Rothbart³

et al. 1995

Journal of Neurosurgery

127

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Peritumoral vasogenic brain edema (PVBE) is a common accompaniment of malignant gliomas. It results from microvascular extravasation of plasma fluid and proteins through the interendothelial spaces. Tumor-associated cysts (TACs) are observed more commonly with benign gliomas that are not associated with PVBE. This study investigates the hypothesis that these morphologically distinct epiphenomena of microvascular extravasation are linked by a common pathophysiological mechanism involving vascular endothelial growth/permeability factor (VEG/PF), which has been implicated in vascular leak phenomena including ascites, malignant effusions, and brain edema. Furthermore, VEG/PF has been isolated from cultured glioma cells, and both VEG/PF protein and messenger RNA transcripts are expressed in brain tumor tissue. To further elucidate the relationship of VEG/PF to PVBE and TACs, the authors examined 34 pathological specimens for VEG/PF expression. Nineteen primary low-grade tumors, 11 primary high-grade tumors, and four gliosis controls were immunostained with a polyclonal anti-VEG/PF immunoglobulin G antibody. Magnetic resonance imaging was used to quantitate PVBE and to determine the presence of TACs and tumor enhancement. The study revealed that eight VEG/PF-negative specimens exhibited no significant edema, whereas 26 VEG/PF-positive tumors exhibited either significant PVBE or TACs. Notably, eight of nine benign TACs that were not associated with PVBE immunostained positive for VEG/PF. These data indicate a high degree of correlation between VEG/PF expression by gliomas and the occurrence of PVBE or TACs, irrespective of tumor grade, thus supporting VEG/PF's pivotal role as the common pathophysiological link between these processes.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

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Vascular endothelial growth/permeability factor expression in human glioma specimens: correlation with vasogenic brain edema and tumor-associated cysts

Strugar¹,

Criscuolo²,

Rothbart³

et al. 1995

Journal of Neurosurgery

127

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“…This suggests that a diffusable factor contributing to BRB breakdown is released by the tumour or in response to the tumour and may have a greater effect on the retinal vasculature than the retinal pigmented epithelium. Breakdown of the structurally similar blood-brain barrier can be mediated by soluble factors released from tumours (Miller et al, 1973;Miyake et al, 1978;Bruce et al, 1987;Connolly et al, 1989aConnolly et al, , 1989bCriscuolo et al, 1990;Criscuolo, 1992).…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical localization of blood-retinal barrier breakdown sites associated with post-surgical macular oedema

et al. 1994

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Post-surgical macular oedema results from blood-retinal barrier breakdown, but it is not accompanied by structural abnormalities in the retinal vessels or retinal pigmented epithelium. Previous studies, using horseradish peroxidase in a primate model, suggested that leakage occurs primarily through this epithelium. This study was conducted to localize sites of the barrier breakdown in humans following different types of intra-ocular surgery and to compare them with eyes affected with ocular inflammatory disease, ocular infection, and choroidal melanoma. Paraffin sections of eyes were immunohistochemically stained for albumin to localize extravascular albumin, which was graded in a masked study. With aphakia/pseudophakia, penetrating keratoplasty, ocular inflammatory disease, ocular infection, and choroidal melanoma, barrier breakdown occurred primarily at the inner blood-retinal barrier (retinal vasculature), but leakage also occurred at the outer barrier (retinal pigmented epithelium). After retinal re-attachment surgery, the inner and outer blood-retinal barriers were equally compromised. Vascular leakage in the optic nerve head coincided with barrier failure in these disorders. The widespread pattern of blood-retinal barrier compromise with leakage at multiple sites suggests that soluble mediators are likely to play a role in postsurgical macular oedema, ocular inflammatory disease, and choroidal melanoma.

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Ultrastructural and Morphometric Investigation of Human Brain Capillaries in Normal and Peritumoral Tissues

Bertossi

Virgintino

Maiorano

et al. 1997

Ultrastructural Pathology

104

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Capillaries of peritumoral and normal brain tissues were ultrastructurally and morphometrically investigated to evaluate the changes in peritumoral capillaries connected with the tumor-associated vasogenic edema. The endothelial cells of peritumoral capillaries showed varying thickness, electron-lucent cytoplasm, and structurally normal tight junctions. The basal lamina was thickened, rarefied, and vacuolated. The pericytes were provided with pinocytotic vesicles and phagocytic bodies. The astrocytic glia appeared empty or swollen, with few glycogen granules and a disarranged cytoskeleton; well-preserved glia was occasionally observed. The brain tissue was slightly edematous. No statistically significant differences were observed between normal and peritumoral capillaries as regards diameter, wall thickness, endothelial thickness, and endothelial vesicle density. Instead, the peritumoral capillaries displayed three times as many endothelial surface-connected vesicles, a markedly thicker basal lamina, and significantly reduced extension of pericytic and glial investments. The kind and severity of the vascular modifications, compared with the slight edematous appearance of the nervous tissue, strengthen the hypothesis that peritumoral capillaries could be involved in the edema resolution process.

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Possible Relationship between Vascular Permeability Factors, Endothelial Cells, and Peritumoral Brain Edema

Cited by 4 publications

References 86 publications

Vascular endothelial growth/permeability factor expression in human glioma specimens: correlation with vasogenic brain edema and tumor-associated cysts

Vascular endothelial growth/permeability factor expression in human glioma specimens: correlation with vasogenic brain edema and tumor-associated cysts

Immunohistochemical localization of blood-retinal barrier breakdown sites associated with post-surgical macular oedema

Ultrastructural and Morphometric Investigation of Human Brain Capillaries in Normal and Peritumoral Tissues

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