Wound repair-induced expression of a stromelysins is associated with the acquisition of a mesenchymal phenotype in human respiratory epithelial cells.

摘要: Wound repair involves many processes including cell migration, provisional matrix deposition, and remodeling. All of these are likely to be affected by matrix-modifying enzymes. Members the metalloproteinases family physiologic mediators extracellular degradation. Within this family, stromelysins can degrade components matrix. We therefore tested hypothesis that could produced human surface respiratory epithelial (HSRE) cells repairing a wound. Experimental wounds were created in vitro HSRE cultures situ bronchial mucosa maintained organ culture. Stromelysin production was measured casein-gel zymography cellular protein extracts derived from migratory nonrepairing stationary wounded cultures. Stromelysin-producing present tissue localized characterized using immunofluorescence techniques. Zymographic techniques showed exclusively cells. Zymogram analysis overexpressed overactivated during wound process, with maximal observed at closure. Using an anti-cytokeratin 14 antibody, we identified stromelysin-3-producing as basal Moreover, most expressed mesenchymal marker vimentin. Similar localization, vimentin-positive located area, they also positive cytokeratin 14. In conclusion, suggested involved migration remodeling repair. Furthermore, stromelysin is linked acquisition phenotype. may then associated shift