Galectin-7 in the Control of Epidermal Homeostasis after Injury.

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Gendronneau, Gaëlle | Sidhu, Sukhvinder S | Delacour, Delphine | Dang, Tien | Calonne, Chloé | Houzelstein, Denis | Magnaldo, Thierry | Poirier, Françoise

Edité par CCSD ; American Society for Cell Biology -

International audience. Monitoring Editor: Benjamin Margolis Galectins, a family of beta-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 which 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. As 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 hyper-proliferative reaction consecutive to both types of stress in galectin-7-deficient mice. Taken together, these studies provide the first genetic evidence showing that galectin-7 can modulate keratinocyte apoptosis, proliferation and migration during skin repair.

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