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J. Biol. Chem., Vol. 276, Issue 38, 35818-35825, September 21, 2001
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From the To gain insight into the molecular mechanisms
underlying cutaneous wound repair, we performed a large scale screen to
identify novel injury-regulated genes. Here we show a strong
up-regulation of the RNA and protein levels of the two
Ca2+-binding proteins S100A8 and S100A9 in the
hyperthickened epidermis of acute murine and human wounds and of human
ulcers. Furthermore, both genes were expressed by inflammatory cells in
the wound. The increased expression of S100A8 and S100A9 in wound
keratinocytes is most likely related to the activated state of the
keratinocytes and not secondary to the inflammation of the skin, since
we also found up-regulation of S100A8 and S100A9 in the epidermis of
activin-overexpressing mice, which develop a hyperproliferative and
abnormally differentiated epidermis in the absence of inflammation.
Furthermore, S100A8 and S100A9 expression was found to be associated
with partially differentiated keratinocytes in vitro. Using
confocal microscopy, both proteins were shown to be at least partially
associated with the keratin cytoskeleton. In addition, cultured
keratinocytes efficiently secreted the S100A8/A9 dimer. These results
together with previously published data suggest that S100A8 and S100A9 are novel players in wound repair, where they might be involved in the
reorganization of the keratin cytoskeleton in the wounded epidermis, in
the chemoattraction of inflammatory cells, and/or in the defense
against microorganisms.
The Ca2+-binding Proteins S100A8 and
S100A9 Are Encoded by Novel Injury-regulated Genes*
,,,,
,,
Institute of Cell Biology, ETH Zürich,
Hönggerberg, CH-8093 Zürich, Switzerland,
§ Institute of Experimental Dermatology, University of
Münster, Von-Esmarch-Str. 56, D-48129 Münster,
¶ SWITCH BIOTECH AG, Fraunhoferstr. 10, D-82152 Martinsried,
Institut für Molekulare Tierzucht und Biotechnologie der
Ludwig-Maximilians-Universität München, Feodor-Lynen-Str.
25, D-81377 München, and ** Klinik für
Dermatologie und Allergologie der Technischen Universität
München am Biederstein, Biedersteiner Str. 29,
D-80802 München, Germany
*
This work was supported by a grant from the
Bundesministerium für Bildung und Forschung (BMBF) (to S. W.,
A. G., and E. W.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Institute of Cell
Biology, HPM D42, ETH Zürich, Hönggerberg, CH-8093
Zürich, Switzerland. Tel.: 0041 1 6333941; Fax: 0041 1 6331174; E-mail: sabine.werner@cell.biol.ethz.ch.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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