title: Increase in the expression of leukocyte elastase inhibitor during wound healing in corneal endothelial cells.
abstract: Tissue injury triggers a complex network of cellular and molecular responses. Although cell migration and proliferation are the most conspicuous, several other responses, such as apoptosis and increased protease activity, are necessary for a proper restitution of the tissue. In this work, we study the leukocyte elastase inhibitor (LEI) expression during wound healing of bovine corneal endothelial monolayers in culture. LEI is a multifunctional protein with anti-protease and anti-apoptotic activity. When properly cleaved, it is transformed into L-DNase II, a pro-apoptotic enzyme and translocated to the nucleus. We found that early after injury LEI increases its protein and mRNA expressions, without nuclear translocation and returns to basal levels immediately after wound closure. This increase is blocked by N-acetylcysteine, suggesting that production of reactive oxygen species immediately after wounding is involved in the LEI increase. Another finding of this work is that there is an acidification of the cells at the wound border which, in contrast to other cell types, does not determine nuclear translocation of the protein. Taken together, the results of this work suggest that the function of LEI during wound healing is related to its activity as a protease inhibitor and/or to its anti-apoptotic activity.
authors.affiliation: Departamento de Bioquímica, Facultad de Medicina, Universidad de la República, Gral. Flores 2125, 11800, Montevideo, Uruguay.
authors.forename: Cristian
authors.initials: C
authors.lastname: Justet
authors.affiliation: Departamento de Bioquímica, Facultad de Medicina, Universidad de la República, Gral. Flores 2125, 11800, Montevideo, Uruguay.|Departamento de Histología y Embriología, Facultad de Medicina, Universidad de la República, Gral. Flores 2125, 11800, Montevideo, Uruguay.
authors.forename: Frances
authors.initials: F
authors.lastname: Evans
authors.affiliation: INSERM U1138, Centre de Recherche des Cordeliers, Paris, France. alicia.torriglia@inserm.fr.|Université Paris Descartes, Paris, France. alicia.torriglia@inserm.fr.|Université Pierre et Marie Curie, Paris, France. alicia.torriglia@inserm.fr.
authors.forename: Alicia
authors.initials: A
authors.lastname: Torriglia
authors.affiliation: Departamento de Bioquímica, Facultad de Medicina, Universidad de la República, Gral. Flores 2125, 11800, Montevideo, Uruguay. schiffle@mednet.org.uy.
authors.forename: Silvia
authors.initials: S
authors.lastname: Chifflet
mesh_terms: D000818:Animals; D020013:Calcium Signaling; D002417:Cattle; D042783:Endothelial Cells / Q000378:metabolism* / Q000473:pathology*; D004728:Endothelium, Corneal / Q000473:pathology*; D005455:Fluorescent Antibody Technique; D006863:Hydrogen-Ion Concentration; D042541:Intracellular Space / Q000378:metabolism; D019272:Leukocyte Elastase / Q000037:antagonists & inhibitors* / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D015843:Serpins / Q000378:metabolism*; D034421:Sus scrofa; D014945:Wound Healing
chemical_list: D017382:Reactive Oxygen Species; D015843:Serpins; D019272:Leukocyte Elastase
keywords: Epithelia; Healing modes; Leukocyte elastase inhibitor; Serpin-B1; Wound healing