Given the remarkable advances in our ability to manipulate the genetic and biochemical behavior of cells and organisms, the previous animal and tissue culture cores have been fused into a Phenotype Core that will assist Center and skin-oriented investigators in the analysis of cell and tissue phenotypes Much of the technology will facilitate the determination of the role of inflammatory mediators and matrix remodeling in skin injury and repair. Cell culture facilities will largely be dedicated to the propagation of well-characterized skin cell strains: keratinocytes, melanocytes, fibroblasts and vascular endothelial cells. Analytic procedures will include routine ELISA and proliferation assays, a novel, high throughput cell migration assay, collagen lattice contraction, and in vitro models of angiogenesis. Whole animal based studies will concentrate on the repair process and animal models thereof. In addition to conventional assessment of incisional and excisional wounds in a number of species, the Phenotype Core will offer investigators a wide variety of humane models for the investigation of matrix formation, angiogenesis, gene therapy and impaired healing. Comprehensive analysis of transgenic animals under the stressed induced by wound repair is often a key tool in determining genotype-phenotype correlations, and the laboratory is fully equipped to determine, in coordination with the other Cores, alterations in wound biomechanics, granulation tissue formation, epithelialization, angiogenesis and matrix accumulation. The analysis emphasize the quantitative aspects of cutaneous wound repair.
| Russell, Shirley B; Smith, Joan C; Huang, Minjun et al. (2015) Pleiotropic Effects of Immune Responses Explain Variation in the Prevalence of Fibroproliferative Diseases. PLoS Genet 11:e1005568 |
| Velez Edwards, Digna R; Tsosie, Krystal S; Williams, Scott M et al. (2014) Admixture mapping identifies a locus at 15q21.2-22.3 associated with keloid formation in African Americans. Hum Genet 133:1513-23 |
| Duncan, F Jason; Silva, Kathleen A; Johnson, Charles J et al. (2013) Endogenous retinoids in the pathogenesis of alopecia areata. J Invest Dermatol 133:334-43 |
| Jandova, Jana; Shi, Mingjian; Norman, Kimberly G et al. (2012) Somatic alterations in mitochondrial DNA produce changes in cell growth and metabolism supporting a tumorigenic phenotype. Biochim Biophys Acta 1822:293-300 |
| Takahashi, Keiko; Mernaugh, Raymond L; Friedman, David B et al. (2012) Thrombospondin-1 acts as a ligand for CD148 tyrosine phosphatase. Proc Natl Acad Sci U S A 109:1985-90 |
| Jandova, Jana; Eshaghian, Alex; Shi, Mingjian et al. (2012) Identification of an mtDNA mutation hot spot in UV-induced mouse skin tumors producing altered cellular biochemistry. J Invest Dermatol 132:421-8 |
| Sundberg, J P; Taylor, D; Lorch, G et al. (2011) Primary follicular dystrophy with scarring dermatitis in C57BL/6 mouse substrains resembles central centrifugal cicatricial alopecia in humans. Vet Pathol 48:513-24 |
| Harries, M J; Sun, J; Paus, R et al. (2010) Management of alopecia areata. BMJ 341:c3671 |
| Yang, Jinming; Splittgerber, Ryan; Yull, Fiona E et al. (2010) Conditional ablation of Ikkb inhibits melanoma tumor development in mice. J Clin Invest 120:2563-74 |
| Russell, Shirley B; Russell, James D; Trupin, Kathryn M et al. (2010) Epigenetically altered wound healing in keloid fibroblasts. J Invest Dermatol 130:2489-96 |
Showing the most recent 10 out of 139 publications
