c-Met is essential for wound healing in the skin

Author:

Chmielowiec Jolanta1,Borowiak Malgorzata2,Morkel Markus1,Stradal Theresia3,Munz Barbara4,Werner Sabine5,Wehland Jürgen3,Birchmeier Carmen2,Birchmeier Walter1

Affiliation:

1. Department of Cancer Biology

2. Department of Neuroscience, Max-Delbrück-Center for Molecular Medicine, 13125 Berlin, Germany

3. Department of Cell Biology, Helmholtz Centre for Infection Research, D-38124 Braunschweig, Germany

4. Institute of Physiology, Charité-Medical University Berlin, 14195 Berlin, Germany

5. Institute of Cell Biology, ETH Zürich, Hönggerberg, CH-8093 Zürich, Switzerland

Abstract

Wound healing of the skin is a crucial regenerative process in adult mammals. We examined wound healing in conditional mutant mice, in which the c-Met gene that encodes the receptor of hepatocyte growth factor/scatter factor was mutated in the epidermis by cre recombinase. c-Met–deficient keratinocytes were unable to contribute to the reepithelialization of skin wounds. In conditional c-Met mutant mice, wound closure was slightly attenuated, but occurred exclusively by a few (5%) keratinocytes that had escaped recombination. This demonstrates that the wound process selected and amplified residual cells that express a functional c-Met receptor. We also cultured primary keratinocytes from the skin of conditional c-Met mutant mice and examined them in scratch wound assays. Again, closure of scratch wounds occurred by the few remaining c-Met–positive cells. Our data show that c-Met signaling not only controls cell growth and migration during embryogenesis but is also essential for the generation of the hyperproliferative epithelium in skin wounds, and thus for a fundamental regenerative process in the adult.

Publisher

Rockefeller University Press

Subject

Cell Biology

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