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First published online March 30, 2007

Journal of Cell Science 120, 802e (2007)
© The Company of Biologists Limited
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In this issue

Wound healing goes to Rac and ruin


Figure 1

During wound healing, increased proliferation of epidermal keratinocytes and their migration across the wound repairs the damaged epithelium. The signalling mechanisms that regulate skin re-epithelialization are poorly understood but there have been hints that the small GTPase Rac1 is involved. Ingo Haase and colleagues now provide the first clear evidence that Rac1 is required for normal epidermal wound healing in vivo in mammals (see p. 1480). Transgenic mice expressing dominant-negative Rac1 (N17Rac1) in epidermal keratinocytes (and mice with an epidermis-specific deletion of Rac1) have a normal epidermis, they report, but repair skin wounds slowly. The authors show that the proliferation and migration of N17Rac1-expressing keratinocytes are both inhibited in vitro, and that the migration defects of these cells are particularly pronounced on collagen. Finally, they report that decreased persistence of lamella protrusions may underlie these migration defects. Overall, these results indicate that Rac1 plays an important role in skin wound healing by regulating keratinocyte proliferation and migration.


Related articles in JCS:

Impaired epidermal wound healing in vivo upon inhibition or deletion of Rac1
Michael Tscharntke, Ruth Pofahl, Anna Chrostek-Grashoff, Neil Smyth, Carien Niessen, Catherin Niemann, Benedikt Hartwig, Volker Herzog, Helmut W. Klein, Thomas Krieg, Cord Brakebusch, and Ingo Haase
JCS 2007 120: 1480-1490. [Abstract] [Full Text]  




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