Journal
JOURNAL OF IMMUNOLOGY
Volume 175, Issue 12, Pages 8337-8345Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.175.12.8337
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Funding
- NHLBI NIH HHS [HL58694] Funding Source: Medline
- NIAID NIH HHS [AI40987] Funding Source: Medline
- NIAMS NIH HHS [AR48267, AR049217] Funding Source: Medline
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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-alpha, and IL-1 beta 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 Mcl-1 is a potential therapeutic target in this disease.
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