DNA degradation during apoptotic cell death.docVIP

Available online /supplements/5/S3 Arthritis Research Therapy Volume 5 Supplement 3, 2003 Meeting abstracts 3rd World Congress of the Global Arthritis Research Network (GARN): International Arthritis Summit Summit Hall at Sheraton Resorts in Miyakazi, Japan 14–17 September 2003 Published online: 12 September 2003 These abstracts are online at /supplements/5/S3 ? 2003 BioMed Central Ltd (Print ISSN 1478-6354; Online ISSN 1478-6362) Plenary Session sis factor alpha, IL-6, and IL-8. The autocrine production of IL-1β by OA cartilage has been of particular interest, since both ex vivo human and in vivo animal studies indicate that IL-1 antagonists effectively attenuate cartilage degradation. Microarray technology has demonstrated differen- tial expression in OA cartilage of a variety of IL-1-induced, NFβB-depen- dent genes. Among IL-β-induced products of OA cartilage are various eicosanoids, which include E , PGD , LTB , PGF , PGF and throm- 1 DNA degradation during apoptotic cell death S Nagata Department of Genetics, Osaka University Medical School, Osaka, Japan 2 2 4 1α 2α boxane. Treatment of OA cartilage with cyclooxygenase (COX) inhibitors Arthritis Res Ther 2003, 5(Suppl 3):1 (DOI 10.1186/ar800) increases LTB production threefold to fivefold, indicating shunting of 4 Apoptosis is a principal mechanism in metazoans by which superfluous or potentially harmful cells are eliminated. Deregulation of this process leads to a variety of diseases such as cancer and autoimmune dis- eases. Stimuli that can induce apoptosis are relatively diverse, and include the death factors (Fas ligand, tumor necrosis factor and TRAIL), DNA damage, and oxidative stress. Regardless of the origin of the apoptotic stimulus, commitment to apoptosis leads to activation of cas- pases, a family of cysteine proteases. Cleavage of a select group of cellular substrates by caspases is responsible for the morphological and biochemic