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Melanoma Associated Chitinase 3-Like 1 Promoted Endothelial Cell Activation and Immune Cell Recruitment

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Melanoma Associated Chitinase 3-Like 1 Promoted Endothelial Cell Activation and Immune Cell Recruitment. / Ramos-Espinosa, Gustavo; Wang, Yuanyuan; Brandner, Johanna M; Schneider, Stefan W; Gorzelanny, Christian.

in: INT J MOL SCI, Jahrgang 22, Nr. 8, 3912, 10.04.2021.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Ramos-Espinosa, G, Wang, Y, Brandner, JM, Schneider, SW & Gorzelanny, C 2021, 'Melanoma Associated Chitinase 3-Like 1 Promoted Endothelial Cell Activation and Immune Cell Recruitment', INT J MOL SCI, Jg. 22, Nr. 8, 3912. https://doi.org/10.3390/ijms22083912

APA

Ramos-Espinosa, G., Wang, Y., Brandner, J. M., Schneider, S. W., & Gorzelanny, C. (2021). Melanoma Associated Chitinase 3-Like 1 Promoted Endothelial Cell Activation and Immune Cell Recruitment. INT J MOL SCI, 22(8), [3912]. https://doi.org/10.3390/ijms22083912

Vancouver

Ramos-Espinosa G, Wang Y, Brandner JM, Schneider SW, Gorzelanny C. Melanoma Associated Chitinase 3-Like 1 Promoted Endothelial Cell Activation and Immune Cell Recruitment. INT J MOL SCI. 2021 Apr 10;22(8). 3912. https://doi.org/10.3390/ijms22083912

Bibtex

@article{b5db3f5b25554458ab56c68336c42f20,
title = "Melanoma Associated Chitinase 3-Like 1 Promoted Endothelial Cell Activation and Immune Cell Recruitment",
abstract = "Chitinase 3-like 1 (CHI3L1) is an enzymatically inactive mammalian chitinase that is associated with tumor inflammation. Previous research indicated that CHI3L1 is able to interact with different extracellular matrix components, such as heparan sulfate. In the present work, we investigated whether the interaction of CHI3L1 with the extracellular matrix of melanoma cells can trigger an inflammatory activation of endothelial cells. The analysis of the melanoma cell secretome indicated that CHI3L1 increases the abundance of various cytokines, such as CC-chemokine ligand 2 (CCL2), and growth factors, such as vascular endothelial growth factor A (VEGF-A). Using a solid-phase binding assay, we found that heparan sulfate-bound VEGF-A and CCL2 were displaced by recombinant CHI3L1 in a dose-dependent manner. Microfluidic experiments indicated that the CHI3L1 altered melanoma cell secretome promoted immune cell recruitment to the vascular endothelium. In line with the elevated VEGF-A levels, CHI3L1 was also able to promote angiogenesis through the release of extracellular matrix-bound pro-angiogenic factors. In conclusion, we showed that CHI3L1 is able to affect the tumor cell secretome, which in turn can regulate immune cell recruitment and blood vessel formation. Accordingly, our data suggest that the molecular targeting of CHI3L1 in the course of cancer immunotherapies can tune patients' response and antitumoral inflammation.",
keywords = "Animals, Blood Vessels/growth & development, Cell Line, Tumor, Chemokine CCL2/genetics, Chitinase-3-Like Protein 1/genetics, Endothelial Cells/immunology, Endothelium, Vascular/growth & development, Extracellular Matrix/drug effects, Gene Expression Regulation, Neoplastic/drug effects, Glycosaminoglycans/pharmacology, HEK293 Cells, Human Umbilical Vein Endothelial Cells, Humans, Melanoma/genetics, Microfluidic Analytical Techniques, Neovascularization, Pathologic/genetics, Protein Binding/genetics, Vascular Endothelial Growth Factor A/genetics",
author = "Gustavo Ramos-Espinosa and Yuanyuan Wang and Brandner, {Johanna M} and Schneider, {Stefan W} and Christian Gorzelanny",
year = "2021",
month = apr,
day = "10",
doi = "10.3390/ijms22083912",
language = "English",
volume = "22",
journal = "INT J MOL SCI",
issn = "1661-6596",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "8",

}

RIS

TY - JOUR

T1 - Melanoma Associated Chitinase 3-Like 1 Promoted Endothelial Cell Activation and Immune Cell Recruitment

AU - Ramos-Espinosa, Gustavo

AU - Wang, Yuanyuan

AU - Brandner, Johanna M

AU - Schneider, Stefan W

AU - Gorzelanny, Christian

PY - 2021/4/10

Y1 - 2021/4/10

N2 - Chitinase 3-like 1 (CHI3L1) is an enzymatically inactive mammalian chitinase that is associated with tumor inflammation. Previous research indicated that CHI3L1 is able to interact with different extracellular matrix components, such as heparan sulfate. In the present work, we investigated whether the interaction of CHI3L1 with the extracellular matrix of melanoma cells can trigger an inflammatory activation of endothelial cells. The analysis of the melanoma cell secretome indicated that CHI3L1 increases the abundance of various cytokines, such as CC-chemokine ligand 2 (CCL2), and growth factors, such as vascular endothelial growth factor A (VEGF-A). Using a solid-phase binding assay, we found that heparan sulfate-bound VEGF-A and CCL2 were displaced by recombinant CHI3L1 in a dose-dependent manner. Microfluidic experiments indicated that the CHI3L1 altered melanoma cell secretome promoted immune cell recruitment to the vascular endothelium. In line with the elevated VEGF-A levels, CHI3L1 was also able to promote angiogenesis through the release of extracellular matrix-bound pro-angiogenic factors. In conclusion, we showed that CHI3L1 is able to affect the tumor cell secretome, which in turn can regulate immune cell recruitment and blood vessel formation. Accordingly, our data suggest that the molecular targeting of CHI3L1 in the course of cancer immunotherapies can tune patients' response and antitumoral inflammation.

AB - Chitinase 3-like 1 (CHI3L1) is an enzymatically inactive mammalian chitinase that is associated with tumor inflammation. Previous research indicated that CHI3L1 is able to interact with different extracellular matrix components, such as heparan sulfate. In the present work, we investigated whether the interaction of CHI3L1 with the extracellular matrix of melanoma cells can trigger an inflammatory activation of endothelial cells. The analysis of the melanoma cell secretome indicated that CHI3L1 increases the abundance of various cytokines, such as CC-chemokine ligand 2 (CCL2), and growth factors, such as vascular endothelial growth factor A (VEGF-A). Using a solid-phase binding assay, we found that heparan sulfate-bound VEGF-A and CCL2 were displaced by recombinant CHI3L1 in a dose-dependent manner. Microfluidic experiments indicated that the CHI3L1 altered melanoma cell secretome promoted immune cell recruitment to the vascular endothelium. In line with the elevated VEGF-A levels, CHI3L1 was also able to promote angiogenesis through the release of extracellular matrix-bound pro-angiogenic factors. In conclusion, we showed that CHI3L1 is able to affect the tumor cell secretome, which in turn can regulate immune cell recruitment and blood vessel formation. Accordingly, our data suggest that the molecular targeting of CHI3L1 in the course of cancer immunotherapies can tune patients' response and antitumoral inflammation.

KW - Animals

KW - Blood Vessels/growth & development

KW - Cell Line, Tumor

KW - Chemokine CCL2/genetics

KW - Chitinase-3-Like Protein 1/genetics

KW - Endothelial Cells/immunology

KW - Endothelium, Vascular/growth & development

KW - Extracellular Matrix/drug effects

KW - Gene Expression Regulation, Neoplastic/drug effects

KW - Glycosaminoglycans/pharmacology

KW - HEK293 Cells

KW - Human Umbilical Vein Endothelial Cells

KW - Humans

KW - Melanoma/genetics

KW - Microfluidic Analytical Techniques

KW - Neovascularization, Pathologic/genetics

KW - Protein Binding/genetics

KW - Vascular Endothelial Growth Factor A/genetics

U2 - 10.3390/ijms22083912

DO - 10.3390/ijms22083912

M3 - SCORING: Journal article

C2 - 33920100

VL - 22

JO - INT J MOL SCI

JF - INT J MOL SCI

SN - 1661-6596

IS - 8

M1 - 3912

ER -