Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tumor Necrosis Factor (TNF) has been implicated in the early metabolic events following acute tissue injury or sepsis; it increases blood levels of glucocorticoids and glucagon or the cellular responses to the hormones. To examine whether stress-related hormones have any effect on macrophage activation by TNF, human monocyte-derived macrophages were exposed to somatostatin (S), ACTH, angiotensin (An), insulin (I), epinephrine (E), and glucagon (G) at physiologic concentrations. 125I-TNF binding as well as the ability of TNF to activate macrophages to kill an intracellular pathogen (Mycobacterium avium) were measured. While treatment with recombinant interferon gamma increased the number of TNF receptors by 53 +/- 8%, E, I, G, S, ACTH and An decreased the number of receptors by 81 +/- 6%, 83 +/- 6%, 15 +/- 5%, 83 +/- 4%, 17 +/- 4% and 21 +/- 4%, respectively. Treatment with I, E, and S also decreased the ability of macrophages to kill M. avium by 30 +/- 1%, 20 +/- 6%, and 51 +/- 2%, respectively. These in vitro results suggest that stress hormones influence TNF-mediated activation of macrophages.
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PMID:Effect of stress-related hormones on macrophage receptors and response to tumor necrosis factor. 197 Oct 32

An increase in apoptotic events may underlie neuropathology in schizophrenia. By data-mining approaches, we identified significant expression changes in death receptor signaling pathways in the dorsolateral prefrontal cortex (DLPFC) of patients with schizophrenia, particularly implicating the Tumor Necrosis Factor Superfamily member 6 (FAS) receptor and the Tumor Necrosis Factor [ligand] Superfamily member 13 (TNFSF13) in schizophrenia. We sought to confirm and replicate in an independent tissue collection the noted mRNA changes with quantitative real-time RT-PCR. To test for regional and diagnostic specificity, tissue from orbital frontal cortex (OFC) was examined and a bipolar disorder group included. In schizophrenia, we confirmed and replicated significantly increased expression of TNFSF13 mRNA in the DLPFC. Also, a significantly larger proportion of subjects in the schizophrenia group had elevated FAS receptor expression in the DLPFC relative to unaffected controls. These changes were not observed in the bipolar disorder group. In the OFC, there were no significant differences in TNFSF13 or FAS receptor mRNA expression. Decreases in BH3 interacting domain death agonist (BID) mRNA transcript levels were found in the schizophrenia and bipolar disorder groups affecting both the DLPFC and the OFC. We tested if TNFSF13 mRNA expression correlated with neuronal mRNAs in the DLPFC, and found significant negative correlations with interneuron markers, parvalbumin and somatostatin, and a positive correlation with PPP1R9B (spinophilin), but not DLG4 (PSD-95). The expression of TNFSF13 mRNA in DLPFC correlated negatively with tissue pH, but decreasing pH in cultured cells did not cause increased TNFSF13 mRNA nor did exogenous TNFSF13 decrease pH. We concluded that increased TNFSF13 expression may be one of several cell-death cytokine abnormalities that contribute to the observed brain pathology in schizophrenia, and while increased TNFSF13 may be associated with lower brain pH, the change is not necessarily causally related to brain pH.
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PMID:Gene expression analysis implicates a death receptor pathway in schizophrenia pathology. 2254 12