Research ExplorerPublicationsEnhanced expression and shedding of the transmembrane chemok...

Enhanced expression and shedding of the transmembrane chemokine CXCL16 by reactive astrocytes and glioma cells

Standard

Enhanced expression and shedding of the transmembrane chemokine CXCL16 by reactive astrocytes and glioma cells. / Ludwig, Andreas; Schulte, Alexander; Schnack, Cathrin; Hundhausen, Christian; Reiss, Karina; Brodway, Neil; Held-Feindt, Janka; Mentlein, Rolf.

In: J NEUROCHEM, Vol. 93, No. 5, 01.06.2005, p. 1293-303.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Ludwig, A, Schulte, A, Schnack, C, Hundhausen, C, Reiss, K, Brodway, N, Held-Feindt, J & Mentlein, R 2005, 'Enhanced expression and shedding of the transmembrane chemokine CXCL16 by reactive astrocytes and glioma cells', J NEUROCHEM, vol. 93, no. 5, pp. 1293-303. https://doi.org/10.1111/j.1471-4159.2005.03123.x

APA

Ludwig, A., Schulte, A., Schnack, C., Hundhausen, C., Reiss, K., Brodway, N., Held-Feindt, J., & Mentlein, R. (2005). Enhanced expression and shedding of the transmembrane chemokine CXCL16 by reactive astrocytes and glioma cells. J NEUROCHEM, 93(5), 1293-303. https://doi.org/10.1111/j.1471-4159.2005.03123.x

Vancouver

Ludwig A, Schulte A, Schnack C, Hundhausen C, Reiss K, Brodway N et al. Enhanced expression and shedding of the transmembrane chemokine CXCL16 by reactive astrocytes and glioma cells. J NEUROCHEM. 2005 Jun 1;93(5):1293-303. https://doi.org/10.1111/j.1471-4159.2005.03123.x

Bibtex

@article{84ab358d3b37484981ebbc4a502b779c,
title = "Enhanced expression and shedding of the transmembrane chemokine CXCL16 by reactive astrocytes and glioma cells",
abstract = "The transmembrane chemokine CXCL16 is expressed by dendritic and vascular cells and mediates chemotaxis and adhesion of activated T cells via the chemokine receptor CXCR6/Bonzo. Here we describe the expression and shedding of this chemokine by glioma cells in situ and in vitro. By quantitative RT-PCR and immunohistochemistry, we show that CXCL16 is highly expressed in human gliomas, while expression in normal brain is low and mainly restricted to brain vascular endothelial cells. In cultivated human glioma cells as well as in activated mouse astroglial cells, CXCL16 mRNA and protein is constitutively expressed and further up-regulated by tumour necrosis factor alpha (TNFalpha) and interferon-gamma (IFNgamma). CXCL16 is continuously released from glial cells by proteolytic cleavage which is rapidly enhanced by stimulation with phorbol-12-myristate-13-acetate (PMA). As shown by inhibitor studies, two distinct members of the disintegrin-like metalloproteinase family ADAM10 and 17 are involved in the constitutive and PMA-induced shedding of glial CXCL16. In addition to the chemokine, its receptor CXCR6 could be detected by quantitative RT-PCR in human glioma tissue, cultivated murine astrocytes and at a lower level in microglial cells. Functionally, recombinant soluble CXCL16 enhanced proliferation of CXCR6-positive murine astroglial and microglial cells. Thus, the transmembrane chemokine CXCL16 is expressed in the brain by malignant and inflamed astroglial cells, shed to a soluble form and targets not only activated T cells but also glial cells themselves.",
keywords = "Animals, Astrocytes, Cell Line, Tumor, Chemokine CXCL6, Chemokines, CXC, Glioma, Humans, Interferon-gamma, Membrane Proteins, Metalloproteases, Mice, Microglia, Neuroglia, RNA, Messenger, Receptors, Immunologic, Receptors, Scavenger, Recombinant Proteins, Solubility, Tissue Culture Techniques, Tumor Necrosis Factor-alpha, Up-Regulation",
author = "Andreas Ludwig and Alexander Schulte and Cathrin Schnack and Christian Hundhausen and Karina Reiss and Neil Brodway and Janka Held-Feindt and Rolf Mentlein",
year = "2005",
month = jun,
day = "1",
doi = "10.1111/j.1471-4159.2005.03123.x",
language = "English",
volume = "93",
pages = "1293--303",
journal = "J NEUROCHEM",
issn = "0022-3042",
publisher = "Wiley-Blackwell",
number = "5",

}

RIS

TY - JOUR

T1 - Enhanced expression and shedding of the transmembrane chemokine CXCL16 by reactive astrocytes and glioma cells

AU - Ludwig, Andreas

AU - Schulte, Alexander

AU - Schnack, Cathrin

AU - Hundhausen, Christian

AU - Reiss, Karina

AU - Brodway, Neil

AU - Held-Feindt, Janka

AU - Mentlein, Rolf

PY - 2005/6/1

Y1 - 2005/6/1

N2 - The transmembrane chemokine CXCL16 is expressed by dendritic and vascular cells and mediates chemotaxis and adhesion of activated T cells via the chemokine receptor CXCR6/Bonzo. Here we describe the expression and shedding of this chemokine by glioma cells in situ and in vitro. By quantitative RT-PCR and immunohistochemistry, we show that CXCL16 is highly expressed in human gliomas, while expression in normal brain is low and mainly restricted to brain vascular endothelial cells. In cultivated human glioma cells as well as in activated mouse astroglial cells, CXCL16 mRNA and protein is constitutively expressed and further up-regulated by tumour necrosis factor alpha (TNFalpha) and interferon-gamma (IFNgamma). CXCL16 is continuously released from glial cells by proteolytic cleavage which is rapidly enhanced by stimulation with phorbol-12-myristate-13-acetate (PMA). As shown by inhibitor studies, two distinct members of the disintegrin-like metalloproteinase family ADAM10 and 17 are involved in the constitutive and PMA-induced shedding of glial CXCL16. In addition to the chemokine, its receptor CXCR6 could be detected by quantitative RT-PCR in human glioma tissue, cultivated murine astrocytes and at a lower level in microglial cells. Functionally, recombinant soluble CXCL16 enhanced proliferation of CXCR6-positive murine astroglial and microglial cells. Thus, the transmembrane chemokine CXCL16 is expressed in the brain by malignant and inflamed astroglial cells, shed to a soluble form and targets not only activated T cells but also glial cells themselves.

AB - The transmembrane chemokine CXCL16 is expressed by dendritic and vascular cells and mediates chemotaxis and adhesion of activated T cells via the chemokine receptor CXCR6/Bonzo. Here we describe the expression and shedding of this chemokine by glioma cells in situ and in vitro. By quantitative RT-PCR and immunohistochemistry, we show that CXCL16 is highly expressed in human gliomas, while expression in normal brain is low and mainly restricted to brain vascular endothelial cells. In cultivated human glioma cells as well as in activated mouse astroglial cells, CXCL16 mRNA and protein is constitutively expressed and further up-regulated by tumour necrosis factor alpha (TNFalpha) and interferon-gamma (IFNgamma). CXCL16 is continuously released from glial cells by proteolytic cleavage which is rapidly enhanced by stimulation with phorbol-12-myristate-13-acetate (PMA). As shown by inhibitor studies, two distinct members of the disintegrin-like metalloproteinase family ADAM10 and 17 are involved in the constitutive and PMA-induced shedding of glial CXCL16. In addition to the chemokine, its receptor CXCR6 could be detected by quantitative RT-PCR in human glioma tissue, cultivated murine astrocytes and at a lower level in microglial cells. Functionally, recombinant soluble CXCL16 enhanced proliferation of CXCR6-positive murine astroglial and microglial cells. Thus, the transmembrane chemokine CXCL16 is expressed in the brain by malignant and inflamed astroglial cells, shed to a soluble form and targets not only activated T cells but also glial cells themselves.

KW - Animals

KW - Astrocytes

KW - Cell Line, Tumor

KW - Chemokine CXCL6

KW - Chemokines, CXC

KW - Glioma

KW - Humans

KW - Interferon-gamma

KW - Membrane Proteins

KW - Metalloproteases

KW - Mice

KW - Microglia

KW - Neuroglia

KW - RNA, Messenger

KW - Receptors, Immunologic

KW - Receptors, Scavenger

KW - Recombinant Proteins

KW - Solubility

KW - Tissue Culture Techniques

KW - Tumor Necrosis Factor-alpha

KW - Up-Regulation

U2 - 10.1111/j.1471-4159.2005.03123.x

DO - 10.1111/j.1471-4159.2005.03123.x

M3 - SCORING: Journal article

C2 - 15934948

VL - 93

SP - 1293

EP - 1303

JO - J NEUROCHEM

JF - J NEUROCHEM

SN - 0022-3042

IS - 5

ER -