title: Amniotic membrane induces epithelialization in massive posttraumatic wounds.
abstract: Large-surface or deep wounds often become senescent in the inflammatory or proliferation stages and cannot progress to reepithelialization. This failure makes intervention necessary to provide the final sealing epithelial layer. The best current treatment is autologous skin graft, although there are other choices such as allogenic or autologous skin substitutes and synthetic dressings. Amniotic membrane (AM) is a tissue of interest as a biological dressing due to its biological properties and immunologic characteristics. It has low immunogenicity and beneficial reepithelialization effects, with antiinflammatory, antifibrotic, antimicrobial, and nontumorigenic properties. These properties are related to its capacity to synthesize and release cytokines and growth factors. We report the use of AM as a wound dressing in two patients with large and deep traumatic wounds. Negative pressure wound therapy followed by AM application was capable of restoring skin integrity avoiding the need for skin graft reconstruction. AM induced the formation of a well-structured epidermis. To understand this effect, we designed some assays on human keratinocyte-derived HaCaT cells. AM treatment of HaCaT induced ERK1/2 and SAP/JNK kinases phosphorylation and c-jun expression, a gene critical for keratinocytes migration; however, it did not affect cell cycle distribution. These data suggest that AM substantially modifies the behavior of keratinocytes in chronic wounds, thereby allowing effective reepithelialization.
authors.affiliation: Unidad de Terapia Celular, Hospital Universitario Virgen de la Arrixaca, El Palmar, Murcia, Spain.
authors.forename: Carmen L
authors.initials: CL
authors.lastname: Insausti
authors.forename: Antonia
authors.initials: A
authors.lastname: Alcaraz
authors.forename: Eva M
authors.initials: EM
authors.lastname: García-Vizcaíno
authors.forename: Anna
authors.initials: A
authors.lastname: Mrowiec
authors.forename: María C
authors.initials: MC
authors.lastname: López-Martínez
authors.forename: Miguel
authors.initials: M
authors.lastname: Blanquer
authors.forename: Antonio
authors.initials: A
authors.lastname: Piñero
authors.forename: María J
authors.initials: MJ
authors.lastname: Majado
authors.forename: José M
authors.initials: JM
authors.lastname: Moraleda
authors.forename: Gregorio
authors.initials: G
authors.lastname: Castellanos
authors.forename: Francisco J
authors.initials: FJ
authors.lastname: Nicolás
mesh_terms: D000368:Aged; D000650:Amnion / Q000637:transplantation*; D001684:Biological Dressings; D001706:Biopsy; D002453:Cell Cycle / Q000502:physiology; D002460:Cell Line / Q000502:physiology; D003131:Combined Modality Therapy; D005260:Female; D006801:Humans; D048031:JNK Mitogen-Activated Protein Kinases / Q000502:physiology; D015603:Keratinocytes / Q000502:physiology; D008875:Middle Aged; D019950:Mitogen-Activated Protein Kinase 1 / Q000502:physiology; D048052:Mitogen-Activated Protein Kinase 3 / Q000502:physiology; D054843:Negative-Pressure Wound Therapy; D010766:Phosphorylation / Q000502:physiology; D016755:Proto-Oncogene Proteins c-jun / Q000502:physiology; D016896:Treatment Outcome; D014945:Wound Healing / Q000502:physiology*; D014950:Wounds, Penetrating / Q000473:pathology / Q000628:therapy*
chemical_list: D016755:Proto-Oncogene Proteins c-jun; D048031:JNK Mitogen-Activated Protein Kinases; C535150:MAPK1 protein, human; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3