Glioblastoma-derived Macrophage Colony-stimulating Factor (MCSF) Induces Microglial Release of Insulin-like Growth Factor-binding Protein 1 (IGFBP1) to Promote Angiogenesis

Nijaguna, Mamatha Bangalore; Patil, Vikas; Urbach, Serge; Shwetha, S; Sravani, K.; Hegde, Anupama; Chandramouli, Bangalore A.; Arivazhagan, Arimappamagan; Marin, Philippe; Santosh, Vani; Somasundaram, Kumaravel

doi:10.1074/jbc.m115.664037

Cited by 73 publications

(63 citation statements)

References 67 publications

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“…IL-6 is able to promote epithelial-mesenchymal transition of cancer cells, which is typically operative in high-grade gliomas. 51 Other paracrine factors that influence the sprouting process include TAM-derived WNT7b and M-CSF in breast cancer and glioma, which can activate the canonical WNT/β-catenin and insulin-like growth factor binding protein pathways, respectively, in endothelial cells, thereby increasing the expression of VEGFA and contributing to vascular sprouting 52,53 (Fig. 2C).…”

Section: Neurooncologymentioning

confidence: 99%

The contribution of tumor-associated macrophages in glioma neo-angiogenesis and implications for anti-angiogenic strategies

et al. 2017

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"Tumor-associated macrophages" (TAMs) form a significant cell population in malignant tumors and contribute to tumor growth, metastasis, and neovascularization. Gliomas are characterized by extensive neo-angiogenesis, and knowledge of the role of TAMs in neovascularization is important for future anti-angiogenic therapies. The phenotypes and functions of TAMs are heterogeneous and more complex than a classification into M1 and M2 inflammation response types would suggest. In this review, we provide an update on the current knowledge of the ontogeny of TAMs, focusing on diffuse gliomas. The role of TAMs in the regulation of the different processes in tumor angiogenesis is highlighted and the most recently discovered mechanisms by which TAMs mediate resistance against current antivascular therapies are mentioned. Novel compounds tested in clinical trials are discussed and brought in relation to different TAM-related angiogenesis pathways. In addition, potential therapeutic targets used to intervene in TAM-regulated tumor angiogenesis are summarized.

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Section: Neurooncologymentioning

confidence: 99%

The contribution of tumor-associated macrophages in glioma neo-angiogenesis and implications for anti-angiogenic strategies

et al. 2017

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“…При ангиогенных заболеваниях, к которым от-носится опухолевый рост, имеет место патологический ангиогенез, в развитии которого особую роль играют фактор роста эндотелия сосудов (VEGF), фактор роста фибробластов (FGF), трансформирующие факторы роста α и ß, которые известны как факторы «запуска» ангиогенеза, и другие факторы [5,6]. Расшифровка важных механизмов ангиогенеза в физиологическом и патологическом состоянии осталась предметом по-вышенного интереса в течение последних 30 лет.…”

Section: Play a Special Role In Its Development Evaluation Of The Imunclassified

“…Авторы показали, что в злокачественных опухолях уровень этого фактора роста был значимо выше, чем в менин-гиомах. Увеличение уровня VEGF в ткани глиобластом показано многочисленными исследованиями [5][6][7][8]. Известно, что VEGF экспрессируются преимуществен-но опухолевыми клетками и в меньшей степени -клетками окружающих тканей глиом [15].…”

Section: результаты и обсуждениеunclassified

“…Эндотелиальные клетки, предназначенные для обра-зования сосудов, оснащены рецепторами этих ангио-генных пептидов [7,17]. Считается, что индукторами VEGF как в норме, так и патологии могут выступать также IGF [6,18].…”

Section: результаты и обсуждениеunclassified

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Some growth factors in neoplastic tissues of brain tumors of different histological structure

Франциянц¹,

Rostorguev²,

Балязин-Парфенов³

et al. 2016

Opuholi golovy šei

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“…Th us, Kim et al (2016) have shown that IGFBP1 and ALDH1A1 are diff erentially overexpressed in the colorectal cancer liver metastasis and may play a dual role, functioning as both tumor suppressors and metastasis promoters in colorectal cancer. Furthermore, there are data that glioblastoma-derived MCSF (macrophage colony-stimulating factor) induces microglial release of IGFBP1 to promote angiogenesis (Nijaguna et al 2015). IGFBP2 is highly up-regulated in glioblastoma tissues.…”

mentioning

confidence: 99%

Expression of genes encoding IGFBPs, SNARK, CD36, and PECAM1 in the liver of mice treated with chromium disilicide and titanium nitride nanoparticles

Minchenko

Tsymbal

Yavorovsky

et al. 2017

Endocrine Regulations

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Objective. Th e aim of the present study was to examine the eff ect of chromium disilicide and titanium nitride nanoparticles on the expression level of genes encoding important regulatory factors (IGFBP1, IGFBP2, IGFBP3, IGFBP4, IGFBP5, SNARK/NUAK2, CD36, and PECAM1/CD31) in mouse liver for evaluation of possible toxic eff ects of these nanoparticles.Methods. Male mice received 20 mg chromium disilicide nanoparticles (45 nm) and titanium nitride nanoparticles (20 nm) with food every working day for 2 months. Th e expression of IGFBP1, IGFBP2, IGFBP3, IGFBP4, IGFBP5, SNARK, CD36, and PECAM1 genes in mouse liver was studied by quantitative polymerase chain reaction.Results. Treatment of mice with chromium disilicide nanoparticles led to down-regulation of the expression of IGFBP2, IGFBP5, PECAM1, and SNARK genes in the liver in comparison with control mice, with more prominent changes for SNARK gene. At the same time, the expression of IGFBP3 and CD36 genes was increased in mouse liver upon treatment with chromium disilicide nanoparticles. We have also shown that treatment with titanium nitride nanoparticles resulted in down-regulation of the expression of IGFBP2 and SNARK genes in the liver with more prominent changes for SNARK gene. At the same time, the expression of IGFBP3, IGFBP4, and CD36 genes was increased in the liver of mice treated with titanium nitride nanoparticles. Furthermore, the effect of chromium disilicide nanoparticles on IGFBP2 and CD36 genes expression was signifi cantly stronger as compared to titanium nitride nanoparticles.Conclusions. Th e results of this study demonstrate that chromium disilicide and titanium nitride nanoparticles have variable eff ects on the expression of IGFBP2, IGFBP3, IGFBP4, IGFBP5, SNARK, CD36, and PECAM1 genes in mouse liver, which may refl ect the genotoxic activities of the studied nanoparticles. A rapid development of nanoscience and nanotechnologies has given a rise to the wide range of applications of man-made nanomaterials in specifi c biomedical fi elds for treatment, diagnosing, controlling, and repairing of biological systems at the molecular level. Titanium nitride nanoparticles have favorable properties and are used for the coating of orthopedic implants, coronary stents, and syringe needles as well as for improving long-term implants in the dental medicine. However, very little is known Unauthenticated Download Date | 5/12/18 12:12 PM

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Glioblastoma-derived Macrophage Colony-stimulating Factor (MCSF) Induces Microglial Release of Insulin-like Growth Factor-binding Protein 1 (IGFBP1) to Promote Angiogenesis

Cited by 73 publications

References 67 publications

The contribution of tumor-associated macrophages in glioma neo-angiogenesis and implications for anti-angiogenic strategies

The contribution of tumor-associated macrophages in glioma neo-angiogenesis and implications for anti-angiogenic strategies

Some growth factors in neoplastic tissues of brain tumors of different histological structure

Expression of genes encoding IGFBPs, SNARK, CD36, and PECAM1 in the liver of mice treated with chromium disilicide and titanium nitride nanoparticles

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