Systemic lupus erythematosus is a multisystem autoimmune disorder of unknown etiology and poorly understood pathogenesis. The heterogeneity of lupus makes it especially difficult to characterize and quantitate in either routine clinical care or in the setting of controlled clinical trials. These problems limit clinical studies of new therapeutic approaches. We propose to apply methods to analyze gene expression using microarrays to characterize patients with lupus with the following specific aims: 1. To compare 7 lupus patients and 3 control subjects for differences in gene expression on gene filter microarrays analyzing 20,000-30,000 gene sequences. 2. To further evaluate groups of related genes suggested by Aim #1 to be of importance in lupus using either selected microarays or RNA (Northern) blot analyses. 3. To examine the gene expression findings for correlations with clinical features, activity and severity of lupus. Studies of gene expression in subjects with lupus offer several advantages over existing approaches. In addition to providing a noninvasive, easily repeatable measure of immune system activation, the results can be quantified and compared for many subjects. More importantly, there is the real possibility of identifying new pathways of immune activation at the molecular level which may in turn suggest approaches to the development of novel therapeutic agents.

Agency
National Institute of Health (NIH)
Institute
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)
Type
Center Core Grants (P30)
Project #
5P30AR041943-08
Application #
6456571
Study Section
Special Emphasis Panel (ZAR1)
Project Start
1994-05-01
Project End
2004-04-30
Budget Start
Budget End
Support Year
8
Fiscal Year
2001
Total Cost
Indirect Cost
Name
Vanderbilt University Medical Center
Department
Type
DUNS #
004413456
City
Nashville
State
TN
Country
United States
Zip Code
37203
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