Expression of vascular endothelial growth factor-b in human astrocytoma

Gollmer, Jean Christophe; Ladoux, Annie; Gioanni, J; Paquis, Philippe; A, Dubreuil; Chatel, M.; Frelin, Christian

doi:10.1215/s1522851799000332

Cited by 8 publications

(10 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…VEGF, a well-described HIF-1␣ target gene, is strongly induced during development but is constitutively expressed at nearly undetectable levels in adulthood under normoxic conditions (2,5,28). VEGF is also upregulated during pathological processes in the brain (28,31,32) and in vitro (8,14,17,39). Indeed hypoxic exposure moderately increased cytoplasmic accumulation and basal release of VEGF in our astrocyte cultures in a time-dependent manner.…”

Section: Discussionmentioning

confidence: 71%

Astrocyte responses to injury: VEGF simultaneously modulates cell death and proliferation

Schmid-Brunclik¹,

Bürgi-Taboada²,

Antoniou³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

Hypoxia is linked to changes in blood-brain barrier (BBB) permeability, and loss of BBB integrity is characteristic of many pathological brain diseases including stroke. In particular, astrocytes play a central role in brain homeostasis and BBB function. We investigated how hypoxia affects astrocyte survival and assessed whether VEGF release through hypoxia-inducible factor-1alpha (HIF-1alpha) induction plays a role in tolerance of these cells to insult. Thus primary astrocytes were subjected to normoxic (21% O(2)), hypoxic (1% O(2)), or near-anoxic (<0.1% O(2)) conditions in the presence or absence of glucose. Cell death was significantly initiated after combined oxygen glucose deprivation, and, surprisingly, astrocyte proliferation increased concomitantly. Near anoxic, but not hypoxic, conditions stabilized HIF-1alpha protein and provoked DNA binding activity, whereas oxygen and glucose deprivation accelerated HIF-1alpha accumulation. Unexpectedly, Hif-1alpha knockdown studies showed that elevated VEGF levels following increased insult was only partially due to HIF-1alpha induction, suggesting alternative mechanisms of VEGF regulation. Notably, endogenous VEGF signaling during insult was essential for cell fate since VEGF inhibition appreciably augmented cell death and reduced proliferation. These data suggest Hif-1 only partially contributes to VEGF-mediated astrocyte responses during chronic injury (as occurs in clinical hypoxic/ischemic insults) that may ultimately be responsible for disrupting BBB integrity.

show abstract

Section: Discussionmentioning

confidence: 71%

Astrocyte responses to injury: VEGF simultaneously modulates cell death and proliferation

Schmid-Brunclik¹,

Bürgi-Taboada²,

Antoniou³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

show abstract

“…VEGF is upregulated by hypoxia, which does not play a role in a cell culture system. However, not all isoform's of VEGF are regulated by hypoxia [45]. Our primer pair for quantitative RT-PCR is not able to distinguish between the different isoform's.…”

Section: Increased Decreasedmentioning

confidence: 89%

Differential gene expression between human schwannoma and control Schwann cells

Hanemann

Bartelt-Kirbach²,

Diebold³

et al. 2006

Neuropathology Appl Neurobio

View full text Add to dashboard Cite

The NF2 gene encodes the tumour suppressor protein merlin. The mutation of a single allele of this gene causes the autosomal dominantly inherited disease neurofibromatosis type 2 (NF2), which is characterized mainly by vestibular schwannoma carrying a second hit mutation. Complete lack of merlin is also found in spontaneous schwannomas and meningiomas. As the events leading to schwannoma development are largely unknown we investigated the differences in gene expression between schwannoma cells from NF2 patients and normal human primary Schwann cells by cDNA array analysis. We identified 41 genes whose expression levels differed by more than factor 2. Most of these clones were corroborated by real-time reverse transcription polymerase chain reaction analysis. By this method a total of seven genes with increased and seven genes with decreased mRNA levels in schwannoma compared with normal Schwann cells could be identified. Regulated clones, some of which not been described in Schwann cells earlier, included matrix metalloproteinase's, growth factors, growth factor receptors and tyrosine kinases.

show abstract

“…Previous studies observed that VEGF-C mRNA was highly expressed in other neurological diseases such as brain tumors (17,18,20,23). Grau et al (18) found that VEGF-C was mainly expressed in endothelial cells and other regions tightly associated with blood vessels in brain tumor tissues.…”

Section: Enhanced Expression Of Vegf-c In Cortical Tubersmentioning

confidence: 98%

Expression and Cellular Distribution of Vascular Endothelial Growth Factor‐C System in Cortical Tubers of the Tuberous Sclerosis Complex

Zhang¹,

Shu²,

Yin³

et al. 2011

Brain Pathology

View full text Add to dashboard Cite

Cortical tubers are malformations of cortical development in patients with tuberous sclerosis complex (TSC), and highly associated with pediatric intractable epilepsy. Recent evidence has shown that signaling mediated through vascular endothelial growth factor-C (VEGF-C) and its receptors, VEGFR-2 and VEGFR-3, has direct effects on both neurons and glial cells. To understand the potential role of VEGF-C system in the pathogenesis of cortical tubers, we investigated the expression patterns of VEGF-C signaling in cortical tubers compared with age-matched normal control cortex (CTX). We found that VEGF-C, VEGFR-2 and VEGFR-3 were clearly upregulated in tubers at both the mRNA and protein levels, compared with CTX. The in situ hybridization and immunostaining results demonstrated that VEGF-C, VEGFR-2 and VEGFR-3 were highly expressed in dysplastic neurons (DNs), giant cells (GCs) and reactive astrocytes within tubers. Most DNs/GCs expressing VEGF-C and its receptors co-labeled with neuronal rather than astrocytic markers, suggesting a neuronal lineage. In addition, protein levels of Akt-1, p-Bad and ERK1/2, the important downstream factors of the VEGF-C pathway, were significantly increased in cortical tubers, indicating involvement of VEGF-C-dependent prosurvival signaling in cortical tubers. Taken together, our results suggest a putative role for the VEGF-C signaling pathway in the pathogenesis of cortical tubers.

show abstract

Expression of vascular endothelial growth factor-b in human astrocytoma

Abstract: Growth of human malignant gliomas is stringently dependent on an angiogenic process that probably involves vascular endothelial growth factor (VEGF). Expressions of

Cited by 8 publications

References 27 publications

Astrocyte responses to injury: VEGF simultaneously modulates cell death and proliferation

Astrocyte responses to injury: VEGF simultaneously modulates cell death and proliferation

Differential gene expression between human schwannoma and control Schwann cells

Expression and Cellular Distribution of Vascular Endothelial Growth Factor‐C System in Cortical Tubers of the Tuberous Sclerosis Complex

Contact Info

Product

Resources

About