Novel Tissue Models of Junctional Epidermolysis Bullosa to Characterize Functional Mechanisms of Sulfur Mustard Injury to Human Skin
Annual rept. 1 May 2002-30 Apr 2003
STATE UNIV OF NEW YORK RESEARCH FOUNDATION AT STONY BROOK OFFICE OF SPONSOREDPROGRAMS
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In the second year of our research, our laboratory has extensively studied skin pathophysiology in response to SM by adapting in vivo, human skinnude mouse chimera to further understand mechanisms of SM-induced vesication of human skin TASK 1. We have established dosetime responses of these skin-like tissues following exposure to SM vapor and have characterized prevesicating and post- vesicating changes in basement membrane and apoptosis that lead to early cell injury and subsequent dermal-epidermal separation. Furthermore, we have developed and tested new tissue models designed to study how basement membrane proteins alter SM-induced selectivity of basal cell injury TASK 8 and how wound response is impaired after SM exposure TASK 6. These studies delineated key factors and pathways that direct the survival and growth of human, skin-like tissues, such as the processing of laminin 5 and activation of AKT signaling, that will now serve as an important baseline for subsequent studies that will determine the effect of SM. In addition, we have refined our organotypic model of wound healing to include components found immediately after SM injury so that effects of SM on reepithelialization can now be studied in a more in vivo-like environment.
- Anatomy and Physiology
- Chemical, Biological and Radiological Warfare