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Circulating angiogenic cells in glioblastoma: toward defining crucial functional differences in CAC-induced neoplastic versus reactive neovascularization.
Neurooncol Adv. 2020 Jan-Dec; 2(1):vdaa040.NA

Abstract

Background

In order to identify suitable therapeutic targets for glioma anti-angiogenic therapy, the process of neovascularization mediated by circulating angiogenic cells (CACs) needs to be scrutinized.

Methods

In the present study, we compared the expression of neovascularization-related genes by 3 circulating CAC subsets (hematopoietic progenitor cells [HPCs], CD34+, and KDR+ cells; internal controls: peripheral blood mononuclear cells and circulating endothelial cells) of treatment-naïve patients with glioblastoma (GBM) to those of patients undergoing reactive neovascularization (myocardial infarction (MI). CACs from umbilical cord (representing developmental neovascularization) and healthy subjects served as controls. Fluorescent-activated cell sorting was used to isolate CACs, RT-PCR to determine the expression levels of a panel of 48 neovascularization-related genes, and Luminex assays to measure plasma levels of 21 CAC-related circulating molecules.

Results

We found essential differences in gene expression between GBM and MI CACs. GBM CACs had a higher expression of proangiogenic factors (especially, KITL, CXCL12, and JAG1), growth factor and chemotactic receptors (IGF1R, TGFBR2, CXCR4, and CCR2), adhesion receptor monomers (ITGA5 and ITGA6), and matricellular factor POSTN. In addition, we found major differences in the levels of neovascularization-related plasma factors. A strong positive correlation between plasma MMP9 levels and expression of CXCR4 in the CAC subset of HPCs was found in GBM patients.

Conclusions

Our findings indicate that CAC-mediated neovascularization in GBM is characterized by more efficient CAC homing to target tissue and a more potent proangiogenic response than in physiologic tissue repair in MI. Our findings can aid in selecting targets for therapeutic strategies acting against GBM-specific CACs.

Authors+Show Affiliations

Laboratory for Tumor Immuno-Pathology, Erasmus Medical Center, Rotterdam, The Netherlands.Laboratory for Tumor Immuno-Pathology, Erasmus Medical Center, Rotterdam, The Netherlands.Department of Pathology and Clinical Bio-Informatics, Erasmus Medical Center, Rotterdam, The Netherlands.Department of Pathology and Clinical Bio-Informatics, Erasmus Medical Center, Rotterdam, The Netherlands.Department of Immunology, Erasmus Medical Center, Rotterdam, The Netherlands.Laboratory for Tumor Immuno-Pathology, Erasmus Medical Center, Rotterdam, The Netherlands.Laboratory for Tumor Immuno-Pathology, Erasmus Medical Center, Rotterdam, The Netherlands.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

32642695

Citation

Huizer, Karin, et al. "Circulating Angiogenic Cells in Glioblastoma: Toward Defining Crucial Functional Differences in CAC-induced Neoplastic Versus Reactive Neovascularization." Neuro-oncology Advances, vol. 2, no. 1, 2020, pp. vdaa040.
Huizer K, Sacchetti A, Swagemakers S, et al. Circulating angiogenic cells in glioblastoma: toward defining crucial functional differences in CAC-induced neoplastic versus reactive neovascularization. Neurooncol Adv. 2020;2(1):vdaa040.
Huizer, K., Sacchetti, A., Swagemakers, S., van der Spek, P. J., Dik, W., Mustafa, D. A., & Kros, J. M. (2020). Circulating angiogenic cells in glioblastoma: toward defining crucial functional differences in CAC-induced neoplastic versus reactive neovascularization. Neuro-oncology Advances, 2(1), vdaa040. https://doi.org/10.1093/noajnl/vdaa040
Huizer K, et al. Circulating Angiogenic Cells in Glioblastoma: Toward Defining Crucial Functional Differences in CAC-induced Neoplastic Versus Reactive Neovascularization. Neurooncol Adv. 2020 Jan-Dec;2(1):vdaa040. PubMed PMID: 32642695.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Circulating angiogenic cells in glioblastoma: toward defining crucial functional differences in CAC-induced neoplastic versus reactive neovascularization. AU - Huizer,Karin, AU - Sacchetti,Andrea, AU - Swagemakers,Sigrid, AU - van der Spek,Peter J, AU - Dik,Wim, AU - Mustafa,Dana A, AU - Kros,Johan M, Y1 - 2020/04/01/ PY - 2020/7/10/entrez PY - 2020/7/10/pubmed PY - 2020/7/10/medline KW - angiogenesis KW - circulating angiogenic cell KW - endothelial progenitor cell KW - glioma KW - hematopoietic progenitor cell KW - myocardial infarction KW - neovascularization SP - vdaa040 EP - vdaa040 JF - Neuro-oncology advances JO - Neurooncol Adv VL - 2 IS - 1 N2 - Background: In order to identify suitable therapeutic targets for glioma anti-angiogenic therapy, the process of neovascularization mediated by circulating angiogenic cells (CACs) needs to be scrutinized. Methods: In the present study, we compared the expression of neovascularization-related genes by 3 circulating CAC subsets (hematopoietic progenitor cells [HPCs], CD34+, and KDR+ cells; internal controls: peripheral blood mononuclear cells and circulating endothelial cells) of treatment-naïve patients with glioblastoma (GBM) to those of patients undergoing reactive neovascularization (myocardial infarction (MI). CACs from umbilical cord (representing developmental neovascularization) and healthy subjects served as controls. Fluorescent-activated cell sorting was used to isolate CACs, RT-PCR to determine the expression levels of a panel of 48 neovascularization-related genes, and Luminex assays to measure plasma levels of 21 CAC-related circulating molecules. Results: We found essential differences in gene expression between GBM and MI CACs. GBM CACs had a higher expression of proangiogenic factors (especially, KITL, CXCL12, and JAG1), growth factor and chemotactic receptors (IGF1R, TGFBR2, CXCR4, and CCR2), adhesion receptor monomers (ITGA5 and ITGA6), and matricellular factor POSTN. In addition, we found major differences in the levels of neovascularization-related plasma factors. A strong positive correlation between plasma MMP9 levels and expression of CXCR4 in the CAC subset of HPCs was found in GBM patients. Conclusions: Our findings indicate that CAC-mediated neovascularization in GBM is characterized by more efficient CAC homing to target tissue and a more potent proangiogenic response than in physiologic tissue repair in MI. Our findings can aid in selecting targets for therapeutic strategies acting against GBM-specific CACs. SN - 2632-2498 UR - https://www.unboundmedicine.com/medline/citation/32642695/Circulating_angiogenic_cells_in_glioblastoma:_toward_defining_crucial_functional_differences_in_CAC-induced_neoplastic_versus_reactive_neovascularization L2 - https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/32642695/ DB - PRIME DP - Unbound Medicine ER -
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