Date of Award

6-22-2007

Degree Type

Thesis

Degree Name

MS Biology

Department

Biology

Advisor

Allan Blake

Committee Member

Jane Ko

Committee Member

Angela Klaus

Keywords

Chronic inflamation, Macrophages, Somatostatin, Somatostatin receptor subtype 2, RAW264.7 cells

Abstract

Chronic inflammation left unchecked can be quite harmful to the tissue with the pro-inflammatory stimulus. It is marked by the recruitment and activation of leukocytes, including lymphocytes and macrophages with their subsequent proliferation and reactive oxygen species release. Macrophages are also one of the primary players in propagating the inflammatory response as they secrete pro-inflammatory cytokines to sustain local tissue responses. Current therapies for chronic inflammation include non-steroidal anti­ inflammatory drugs and glucocorticoids; however, both have various side effects and setbacks. Somatostatin is an endogenous hormone which inhibits cellular secretion and proliferation throughout the body. Somatostatin receptor activation is mediated through a family of heterotrimeric guanine nucleotide coupled proteins (G-proteins) belonging to the Gi and G0 family of G-proteins. In this study, we show that a murine macrophage cell line, RA W264.7, transcribes the mRNA and expresses the protein of the somatostatin receptor 2B subtype. We also demonstrate that this receptor reduces cytokine-induced phosphorylation of the ST A T-3 transcription factor. Taken together, these data suggest the functional presence of a somatostatin receptor in the RAW 264. 7 macrophage cell, a cellular model of the murine macrophage.

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