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Vol. 19, Issue 12, 5541-5549, December 2008

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Galectin-7 in the Control of Epidermal Homeostasis after Injury

Gaëlle Gendronneau^*,, Sukhvinder S. Sidhu^*,, Delphine Delacour^*, Tien Dang^*, Chloé Calonne^*, Denis Houzelstein^*, Thierry Magnaldo, and Françoise Poirier^*

*Institut Jacques Monod, Unité Mixte de Recherche Centre National de la Recherche Scientifique 7592, Universités Paris 6 and Paris 7, 75251 Paris Cedex 5, France; and Institut Gustave Roussy, Genetic Instability and Cancer Unit, Centre National de la Recherche Scientifique Formation de Recherche en Evolution 2939, 94805 Villejuif Cedex, France

Submitted February 15, 2008; Revised September 2, 2008; Accepted September 19, 2008
Monitoring Editor: Benjamin Margolis

Galectins, a family of β-galactoside binding lectins, have recently emerged as novel regulators of tissue homeostasis. Galectin-7 is predominantly expressed in stratified epithelia, especially in epidermis. We report here the generation of galectin-7–deficient mice that are viable and do not display phenotypical abnormalities in skin structure or expression of epidermal markers. However, these mice show unique defects in the maintenance of epidermal homeostasis in response to environmental challenges. First, after UVB irradiation in vivo, the apoptotic response is prematurely triggered and lasts longer in the mutant epidermis. This result contrasts with the proapoptotic role that had been proposed for galectin-7. Second, wound-healing experiments in vivo revealed that galectin-7–deficient mice displayed a reduced reepithelialization potential compared with wild-type littermates. This effect could be attributed to a defect in cell migration. Because galectin-7 is located in the podosomes of keratinocytes migrating out of skin explants in culture, we propose that this glycan-binding protein may directly influence cell/extracellular matrix interactions. Finally, we also detected an unexpected intense hyperproliferative reaction consecutive to both types of stress in galectin-7–deficient mice. Together, these studies provide the first genetic evidence showing that galectin-7 can modulate keratinocyte apoptosis, proliferation, and migration during skin repair.

These authors contributed equally to this work.

Address correspondence to: Françoise Poirier (poirier{at}ijm.jussieu.fr).

Abbreviations used: Ab, antibody; ECM, extracellular matrix; CRD, carbohydrate recognition domain; UV, ultraviolet; wt, wild type.