Vascular Gene Expression in Nonneoplastic and Malignant Brain

Madden, Stephen L.; Cook, Brian P.; Nacht, Mariana; Weber, William; Callahan, Michelle; Jiang, Yingjie; Dufault, Michael R.; Zhang, Xiaoming; Zhang, Wen; Walter-Yohrling, Jennifer; Rouleau, Cecile; Akmaev, Viatcheslav R.; Wang, Clarence J.; Cao, Xiaohong; Martin, Thia B. St.; Roberts, Bruce; Teicher, Beverly A.; Klinger, Katherine W.; Stan, Radu V.; Lucey, Brendan P.; Carson-Walter, Eleanor B.; Laterra, John; Walter, Kevin A.

doi:10.1016/s0002-9440(10)63324-x

Cited by 166 publications

(158 citation statements)

References 27 publications

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“…However, the molecular mechanisms that control endosialin expression have remained elusive (Rettig et al, 1992;Brady et al, 2004;Davies et al, 2004;Madden et al, 2004;Dolznig et al, 2005;MacFadyen et al, 2005;Huber et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

“…Subsequent studies have confirmed that endosialin is upregulated in blood vessels and activated stromal fibroblasts in human colorectal, brain and breast tumours as well as in mouse xenograft models (Carson-Walter et al, 2001;Brady et al, 2004;Davies et al, 2004;Madden et al, 2004;Dolznig et al, 2005;MacFadyen et al, 2005MacFadyen et al, , 2007Huber et al, 2006;Rupp et al, 2006). Endosialin expression is restricted to capillaries and shows a heterogeneous pattern typical for molecules involved in vascular reorganisation.…”

mentioning

confidence: 92%

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Hypoxia upregulates expression of human endosialin gene via hypoxia-inducible factor 2

et al. 2008

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Endosialin is a transmembrane glycoprotein selectively expressed in blood vessels and stromal fibroblasts of various human tumours. It has been functionally implicated in angiogenesis, but the factors that control its expression have remained unclear. As insufficient delivery of oxygen is a driving force of angiogenesis in growing tumours, we investigated whether hypoxia regulates endosialin expression. Here, we demonstrate that endosialin gene transcription is induced by hypoxia predominantly through a mechanism involving hypoxia-inducible factor-2 (HIF-2) cooperating with the Ets-1 transcription factor. We show that HIF-2 activates the endosialin promoter both directly, through binding to a hypoxia-response element adjacent to an Ets-binding site in the distal part of the upstream regulatory region, and indirectly, through Ets-1 and its two cognate elements in the proximal promoter. Our data also suggest that the SP1 transcription factor mediates responsiveness of the endosialin promoter to high cell density. These findings elucidate important aspects of endosialin gene regulation and provide a rational frame for future investigations towards better understanding of its biological significance.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 92%

Hypoxia upregulates expression of human endosialin gene via hypoxia-inducible factor 2

et al. 2008

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“…Recently, a new SDF-1 receptor named CXCR7 has been discovered [66,67]. CXCR7 is also expressed on tumor cells and endothelium and regulates tumor growth [67,68]. As such, it is conceivable that CXCR4-independent effects of SDF-1 on angiogenesis could potentially be attributed to CXCR7 [69].…”

Section: Multiples Roles Of Sdf-1 In Governing Neo-angiogenesis In Vivomentioning

confidence: 99%

The SDF-1–CXCR4 signaling pathway: a molecular hub modulating neo-angiogenesis

Petit

Jin

Rafii

2007

Trends in Immunology

530

382

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Pro-angiogenic bone marrow (BM) cells include subsets of hematopoietic cells that provide vascular support and endothelial progenitor cells (EPCs), which under certain permissive conditions could differentiate into functional vascular cells. Recent evidence demonstrates that the chemokine stromal-cell derived factor-1 (SDF-1, also known as CXCL12) has a major role in the recruitment and retention of CXCR4 + BM cells to the neo-angiogenic niches supporting revascularization of ischemic tissue and tumor growth. However, the precise mechanism by which activation of CXCR4 modulates neo-angiogenesis is not clear. SDF-1 not only promotes revascularization by engaging with CXCR4 expressed on the vascular cells but also supports mobilization of pro-angiogenic CXCR4 + VEGFR1 + hematopoietic cells, thereby accelerating revascularization of ischemic organs. Here, we attempt to define the multiple functions of the SDF-1-CXCR4 signaling pathway in the regulation of neo-vascularization during acute ischemia and tumor growth. In particular, we introduce the concept that, by modulating plasma SDF-1 levels, the CXCR4 antagonist AMD3100 acutely promotes, while chronic AMD3100 treatment inhibits, mobilization of pro-angiogenic cells. We will also discuss strategies to modulate the mobilization of essential subsets of BM cells that participate in neo-angiogenesis, setting up the stage for enhancing revascularization or targeting tumor vessels by exploiting CXCR4 agonists and antagonists, respectively.

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“…Dwyer et al demonstrated that IL-8 has the ability to function as an angiogenic factor in glioblastoma (Dwyer et al, 2012). CXCR7 is reported to be upregulated in blood vessels of malignant brain tumors and mediates the recruitment of endothelial cells to the SDF-1 secreted tumor cells (Madden et al, 2004).…”

Section: Expression Of Chemokines and Chemokine Receptors In Brain Tumentioning

confidence: 99%

Expression of Chemokines and Chemokine Receptors in Brain Tumor Tissue Derived Cells

Razmkhah

Arabpour²,

Taghipour³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Chemokine and chemokine receptor expression by tumor cells contributes to tumor growth and angiogenesis and thus these factors may be considered as tumor markers. Here we aimed to characterize cells directly extracted from glioma, meningioma, and secondary brain tumors as well as non-tumoral cells in vitro. Cells were isolated from brain tissues using 0.2% collagenase and characterized by flow cytometry. Expression of SDF-1, CXCR4, CXCR7, RANTES, CCR5, MCP-1 and IP-10 was defined using flow cytometry and qRT-PCR methods. Brain tissue isolated cells were observed as spindle-shaped cell populations. No significant differences were observed for expression of SDF-1, CXCR4, CXCR7, RANTES, CCR5, and IP-10 transcripts. However, the expression of CXCR4 was approximately 13-fold and 110-fold higher than its counterpart, CXCR7, in meningioma and glioma cells, respectively. CXCR7 was not detectable in secondary tumors but CXCR4 was expressed. In non tumoral cells, CXCR7 had 1.3-fold higher mRNA expression than CXCR4. Flow cytometry analyses of RANTES, MCP-1, IP-10, CCR5 and CXCR4 expression showed no significant difference between low and high grade gliomas. Differential expression of CXCR4 and CXCR7 in brain tumors derived cells compared to non-tumoral samples may have crucial impacts on therapeutic interventions targeting the SDF-1/CXCR4/CXCR7 axis.

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Vascular Gene Expression in Nonneoplastic and Malignant Brain

Cited by 166 publications

References 27 publications

Hypoxia upregulates expression of human endosialin gene via hypoxia-inducible factor 2

Hypoxia upregulates expression of human endosialin gene via hypoxia-inducible factor 2

The SDF-1–CXCR4 signaling pathway: a molecular hub modulating neo-angiogenesis

Expression of Chemokines and Chemokine Receptors in Brain Tumor Tissue Derived Cells

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