Abstract
Somatostatin (somatotropin release inhibitory factor; SRIF) peptides are widely distributed in the mammalian body and, acting through a family of genetically homologous cell surface receptors (sst1-5), regulate cellular secretion and proliferation. Compelling evidence implicates SRIF peptides and peptidyl analogues in chronic inflammatory diseases such as rheumatoid arthritis (RA). SRIF membrane receptors exist on immune and synovial cells, thereby providing molecular targets on the principal participants in the RA pro-inflammatory cascade. Preclinical and clinical studies have shown that SRIF peptides and analogues are anti-inflammatory, however the cellular basis for this activity remains unclear. Since RA inflammation is propagated through cell-mediated immune responses which orchestrate the proinflammatory cytokine production by monocytes, macrophages and synovial fibroblasts, SRIF could provide a strategy for interrupting RA progression. SRIF and SRIF analogues reduce synoviocyte proliferation and suppress synovial cytokine production, thereby making SRIF analogues a potentially novel approach to RA treatment. This review summarizes our current knowledge of SRIF analogue therapies in RA.
Keywords: metalloproteinases, Somatostatin Receptor Subtype, Synovium, inflammatory cascade, SRIF modulation
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