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* Division of Rheumatology, Northwestern University Feinberg School of Medicine and The Jesse Brown Veterans Affairs Chicago Heathcare System, and
Department of Pathology and
Department of Microbiology and Immunology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611;
Department of Molecular Microbiology and Immunology, Saint Louis University Medical School, St. Louis, MO 63104; and
¶
Department of Medicine, Rheumatology Division, University of Michigan and Ann Arbor Veterans Affairs Medical Center, Ann Arbor, MI 48109
Mcl-1 is a Bcl-2-family, antiapoptotic molecule that is critical for the survival of T and B lymphocytes and macrophages; however, its role in nonhemopoietic cells remains to be fully elucidated. The current study focuses on the role of Mcl-1 in rheumatoid arthritis (RA). Mcl-1 was strongly expressed in the synovial lining and was increased in the sublining fibroblasts of patients with RA, compared with control synovial tissue. The expression of Mcl-1 in sublining fibroblasts correlated with the degree of inflammation and TNF-
, and IL-1
treatment of cultured synovial fibroblasts resulted in the increased expression of Mcl-1 at the mRNA and protein levels. Mcl-1 was critical for the survival of RA synovial fibroblasts, because the forced reduction of Mcl-1 using a Mcl-1 antisense-expressing adenoviral vector induced apoptotic cell death, which was mediated through Bax, Bak, and Bim. These observations document a critical role for Mcl-1 in protecting against apoptosis in RA and suggest that Mc1–1 is a potential therapeutic target in this disease.
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