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Somatostatin regulates intracellular signaling in rheumatoid arthritis synoviocytes *
Author(s) -
West Frances Mae,
Belin Kari A.,
Blake Allan D.
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a971-d
Subject(s) - somatostatin , somatostatin receptor , chemistry , receptor , intracellular , signal transduction , extracellular , medicine , somatostatin receptor 2 , endocrinology , microbiology and biotechnology , biology , biochemistry
Somatostatin (somatotropin release inhibitory factor, SRIF) is widely expressed in the body, where it controls cell proliferation and secretion via a family of highly homologous G protein‐coupled receptors (GPCRs). SRIF analogs have demonstrated clinical utility in a range of endocrine, neuroendocrine and inflammatory disorders. We have investigated the role of SRIF in modulating the inflammatory response of the human synoviocyte, a critical cell in rheumatoid arthritis (RA). We utilized SRIF receptor‐specific oligonucleotide primers to perform reverse transcriptase‐polymerase chain reaction (RT‐PCR) on synovial mRNA, thus identifying a molecular target for synovial SRIF action. Immunoblotting experiments with phospho‐specific antiserum showed that SRIF controlled the ERK1/2 extracellular regulated kinases in rheumatoid synoviocytes. In addition, SRIF suppresses sodium vanadate sensitive protein tyrosine phosphatase activity as measured with the fluorescent substrate, 6,8 difluor‐4‐methylumbelliferryll phosphate (DiF MUP; Invitrogen, Carlsbad, CA). Taken together our results demonstrate that SRIF regulates intracellular signaling in rheumatoid synoviocytes.