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Biological Technologies (M.T.F., L.W., A.J.D.) and Cardiovascular and Metabolic Diseases (J.C.K.), Wyeth Research, Cambridge, Massachusetts 02140; Caprion Pharmaceuticals (M.P., D.C., C.H., P.K., P.T., E.P.), Montréal, Québec, Canada H4S 2C8; and Women’s Health Research Institute (H.A.H.), Wyeth Research, Collegeville, Pennsylvania 19426
Address all correspondence and requests for reprints to: Heather A. Harris, Wyeth Research, Women’s Health Research Institute, RN-3256, 500 Arcola Road, Collegeville, Pennsylvania 19426. E-mail: harrish{at}wyeth.com.
Two receptors [estrogen receptor (ER)
and ERß] mediate the manifold effects of estrogens throughout the body. Although a clear role has been established for ER in the classical effects of estrogen activity, the physiological role of ERß is less well understood. A small-molecule ERß selective agonist, ERB-041, has potent antiinflammatory activity in the Lewis rat model of adjuvant-induced arthritis. To characterize the response of target organs and pathways responsible for this antiinflammatory effect, mRNA expression profiling of the spleen, lymph node, and liver was performed, in conjunction with a global analysis of the plasma proteome. We find that the expression of a large number of genes and proteins are altered in the disease model and the majority of these are partially or fully reversed by ERB-041 treatment. Regulated pathways include the acute-phase response, eicosanoid synthesis, fatty acid metabolism, and iron metabolism. In addition, many of the regulated genes and proteins are known to be dysregulated in human rheumatoid arthritis, providing further evidence that the manifestations of the Lewis rat adjuvant-induced arthritis model bear similarity to the human disease.
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