Glioblastoma cell-secreted interleukin-8 induces brain endothelial cell permeability via CXCR2.

Glioblastoma constitutes the most aggressive and deadly of brain tumors. As yet, both conventional and molecular-based therapies have met with limited success in treatment of this cancer. Among other explanations, the heterogeneity of glioblastoma and the associated microenvironment contribute to it...

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Autores principales:	Julie Dwyer, Jagoda K Hebda, Armelle Le Guelte, Eva-Maria Galan-Moya, Sherri S Smith, Sandy Azzi, Nicolas Bidere, Julie Gavard
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/586ebc2991014042904bb799e4964e01
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spelling	oai:doaj.org-article:586ebc2991014042904bb799e4964e012021-11-18T07:04:43ZGlioblastoma cell-secreted interleukin-8 induces brain endothelial cell permeability via CXCR2.1932-620310.1371/journal.pone.0045562https://doaj.org/article/586ebc2991014042904bb799e4964e012012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23029099/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Glioblastoma constitutes the most aggressive and deadly of brain tumors. As yet, both conventional and molecular-based therapies have met with limited success in treatment of this cancer. Among other explanations, the heterogeneity of glioblastoma and the associated microenvironment contribute to its development, as well as resistance and recurrence in response to treatments. Increased vascularity suggests that tumor angiogenesis plays an important role in glioblastoma progression. However, the molecular crosstalk between endothelial and glioblastoma cells requires further investigation. To examine the effects of glioblastoma-derived signals on endothelial homeostasis, glioblastoma cell secretions were collected and used to treat brain endothelial cells. Here, we present evidence that the glioblastoma secretome provides pro-angiogenic signals sufficient to disrupt VE-cadherin-mediated cell-cell junctions and promote endothelial permeability in brain microvascular endothelial cells. An unbiased angiogenesis-specific antibody array screen identified the chemokine, interleukin-8, which was further demonstrated to function as a key factor involved in glioblastoma-induced permeability, mediated through its receptor CXCR2 on brain endothelia. This underappreciated interface between glioblastoma cells and associated endothelium may inspire the development of novel therapeutic strategies to induce tumor regression by preventing vascular permeability and inhibiting angiogenesis.Julie DwyerJagoda K HebdaArmelle Le GuelteEva-Maria Galan-MoyaSherri S SmithSandy AzziNicolas BidereJulie GavardJulie GavardPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 9, p e45562 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Julie Dwyer Jagoda K Hebda Armelle Le Guelte Eva-Maria Galan-Moya Sherri S Smith Sandy Azzi Nicolas Bidere Julie Gavard Julie Gavard Glioblastoma cell-secreted interleukin-8 induces brain endothelial cell permeability via CXCR2.
description	Glioblastoma constitutes the most aggressive and deadly of brain tumors. As yet, both conventional and molecular-based therapies have met with limited success in treatment of this cancer. Among other explanations, the heterogeneity of glioblastoma and the associated microenvironment contribute to its development, as well as resistance and recurrence in response to treatments. Increased vascularity suggests that tumor angiogenesis plays an important role in glioblastoma progression. However, the molecular crosstalk between endothelial and glioblastoma cells requires further investigation. To examine the effects of glioblastoma-derived signals on endothelial homeostasis, glioblastoma cell secretions were collected and used to treat brain endothelial cells. Here, we present evidence that the glioblastoma secretome provides pro-angiogenic signals sufficient to disrupt VE-cadherin-mediated cell-cell junctions and promote endothelial permeability in brain microvascular endothelial cells. An unbiased angiogenesis-specific antibody array screen identified the chemokine, interleukin-8, which was further demonstrated to function as a key factor involved in glioblastoma-induced permeability, mediated through its receptor CXCR2 on brain endothelia. This underappreciated interface between glioblastoma cells and associated endothelium may inspire the development of novel therapeutic strategies to induce tumor regression by preventing vascular permeability and inhibiting angiogenesis.
format	article
author	Julie Dwyer Jagoda K Hebda Armelle Le Guelte Eva-Maria Galan-Moya Sherri S Smith Sandy Azzi Nicolas Bidere Julie Gavard Julie Gavard
author_facet	Julie Dwyer Jagoda K Hebda Armelle Le Guelte Eva-Maria Galan-Moya Sherri S Smith Sandy Azzi Nicolas Bidere Julie Gavard Julie Gavard
author_sort	Julie Dwyer
title	Glioblastoma cell-secreted interleukin-8 induces brain endothelial cell permeability via CXCR2.
title_short	Glioblastoma cell-secreted interleukin-8 induces brain endothelial cell permeability via CXCR2.
title_full	Glioblastoma cell-secreted interleukin-8 induces brain endothelial cell permeability via CXCR2.
title_fullStr	Glioblastoma cell-secreted interleukin-8 induces brain endothelial cell permeability via CXCR2.
title_full_unstemmed	Glioblastoma cell-secreted interleukin-8 induces brain endothelial cell permeability via CXCR2.
title_sort	glioblastoma cell-secreted interleukin-8 induces brain endothelial cell permeability via cxcr2.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/586ebc2991014042904bb799e4964e01
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Glioblastoma cell-secreted interleukin-8 induces brain endothelial cell permeability via CXCR2.

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