Galectin-7 in the Control of Epidermal Homeostasis after Injury
Galectin-7 in the Control of Epidermal Homeostasis after Injury
复制标题
DOI：
10.1091/mbc.e08-02-0166
复制
发表时间：
2008-12-01
影响因子：
3.3
通讯作者：
Poirier, Francoise
中科院分区：
文献类型：
--
作者：
Gendronneau, Gaelle;Sidhu, Sukhvinder S.;Poirier, Francoise
半乳糖凝集素是β -半乳糖苷结合凝集素的一个家族，最近作为组织稳态的新调节因子出现。半乳糖凝集素-7主要表达于层状上皮，尤其是表皮。我们在这里报道了半乳糖凝集素-7缺陷小鼠的产生，这些小鼠是可行的，并且在皮肤结构或表皮标记物的表达方面没有表现出表型异常。然而，这些小鼠在应对环境挑战时在维持表皮稳态方面表现出独特的缺陷。首先，在体内UVB照射后，凋亡反应在突变体表皮中过早触发并持续更长时间。这一结果与半乳糖凝集素-7的促凋亡作用形成对比。其次，体内伤口愈合实验显示，与野生型小鼠相比，半乳糖凝集素-7缺陷小鼠的再上皮化潜力降低。这种效应可能归因于细胞迁移的缺陷。由于半乳糖凝集素-7位于培养中从皮肤外植体迁移出来的角质形成细胞的足小体中，我们提出这种聚糖结合蛋白可能直接影响细胞/细胞外基质的相互作用。最后，我们还在半乳糖凝集素-7缺乏的小鼠中发现了连续的两种应激类型的意想不到的强烈超增殖反应。总之，这些研究提供了第一个遗传学证据，表明半乳糖凝集素-7可以调节皮肤修复过程中角质细胞的凋亡、增殖和迁移。
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 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.