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Biological Chemistry

Editor-in-Chief: Brüne, Bernhard

Editorial Board: Buchner, Johannes / Lei, Ming / Ludwig, Stephan / Thomas, Douglas D. / Turk, Boris / Wittinghofer, Alfred


IMPACT FACTOR 2018: 3.014
5-year IMPACT FACTOR: 3.162

CiteScore 2018: 3.09

SCImago Journal Rank (SJR) 2018: 1.482
Source Normalized Impact per Paper (SNIP) 2018: 0.820

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1437-4315
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Volume 393, Issue 5

Issues

Kallikrein 6 is a novel molecular trigger of reactive astrogliosis

Isobel A. Scarisbrick
  • Neurobiology of Disease Program, Mayo Medical and Graduate School, Rochester, MN 55905, USA
  • Department of Physical Medicine and Rehabilitation, Mayo Medical and Graduate School, Rochester, MN 55905, USA
  • Department of Neurology, Mayo Medical and Graduate School, Rochester, MN 55905, USA
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  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Maja Radulovic / Joshua E. Burda / Nadya Larson
  • Department of Physical Medicine and Rehabilitation, Mayo Medical and Graduate School, Rochester, MN 55905, USA
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  • De Gruyter OnlineGoogle Scholar
/ Sachiko I. Blaber
  • Department of Biomedical Sciences, Florida State University College of Medicine, Tallahassee, FL 32306-4300, USA
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  • De Gruyter OnlineGoogle Scholar
/ Caterina Giannini / Michael Blaber
  • Department of Biomedical Sciences, Florida State University College of Medicine, Tallahassee, FL 32306-4300, USA
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  • De Gruyter OnlineGoogle Scholar
/ Alexander G. Vandell

Abstract

Kallikrein-related peptidase 6 (KLK6) is a trypsin-like serine protease upregulated at sites of central nervous system (CNS) injury, including de novo expression by reactive astrocytes, yet its physiological actions are largely undefined. Taken with recent evidence that KLK6 activates G-protein-coupled protease-activated receptors (PARs), we hypothesized that injury-induced elevations in KLK6 contribute to the development of astrogliosis and that this occurs in a PAR-dependent fashion. Using primary murine astrocytes and the Neu7 astrocyte cell line, we show that KLK6 causes astrocytes to transform from an epitheliod to a stellate morphology and to secrete interleukin 6 (IL-6). By contrast, KLK6 reduced expression of glial fibrillary acidic protein (GFAP). The stellation-promoting activities of KLK6 were shown to be dependent on activation of the thrombin receptor, PAR1, as a PAR1-specific inhibitor, SCH79797, blocked KLK6-induced morphological changes. The ability of KLK6 to promote astrocyte stellation was also shown to be linked to activation of protein kinase C (PKC). These studies indicate that KLK6 is positioned to serve as a molecular trigger of select physiological processes involved in the development of astrogliosis and that this is likely to occur at least in part by activation of the G-protein-coupled receptor, PAR1.

Keywords: astrocyte; GFAP; glioblastoma; IL-6; multiple sclerosis; protease-activated receptor; spinal cord injury

About the article

Corresponding author


Received: 2011-10-31

Accepted: 2012-01-20

Published in Print: 2012-05-01


Citation Information: , Volume 393, Issue 5, Pages 355–367, ISSN (Online) 1437-4315, ISSN (Print) 1431-6730, DOI: https://doi.org/10.1515/hsz-2011-0241.

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