© 2003 BMJ Publishing Group Ltd. & Association of Clinical Pathologists
ECHO
Protein kinase regulates IL16 transcription in arthritis
| The first 150 words of the full text of this article appear below. |
Molecular researchers have suggested that pathways dependent on protein kinase C may regulate transcription of interleukin 16 (IL16), a proinflammatory cytokine abundant in arthritic joints.
They compared the effect of various chemical agents on steady state (IL16) mRNA transcripts in growing synovial fibroblasts from six patients with rheumatoid arthritis (RA) and three with osteoarthritis (OA). The reverse transcriptase PCR method they used enabled them to obtain results that were semiquantitative.
Early passage synovial fibroblasts from patients with RA or OA transcribed IL16 mRNA when incubated with growing medium without additives. Protein kinase inhibitor staurosporine enhanced IL16 steady state mRNA in both types of synovial fibroblasts and specific protein kinase C activator phorbol-12-myristate-13-acetate reduced transcription. Other agents—the calcium ionophore ionomycin, protein kinase A stimulator cyclic AMP, and G protein activator MAS-7—gave minor, variable responses. Phosphatase inhibitor okadaic acid and protein kinase inhibitor H-7 dihydrochloride reduced mRNA transcripts, maybe because of their
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
- Full Text
- Full Text (PDF)
- Submit a response
- Alert me when this article is cited
- Alert me when eLetters are posted
- Alert me if a correction is posted
Services
- Email this link to a friend
- Similar articles in this journal
- Add article to my folders
- Download to citation manager
- Request Permissions
