title: Regulation of apoptosis by somatostatin and substance P in peritoneal macrophages.
abstract: Recent studies have shown that somatostatin (SOM) inhibits interleukin 6 (IL-6) and interferon gamma (IFNgamma) production by lymphocytes and peritoneal macrophages, whereas substance P (SP) enhances these cytokines production. To define the mechanism of the cytokine production enhancements and inhibitions by SOM and SP, we examined the expression of apoptosis modulator, p53, Bcl-2, Bax, inducible nitric oxide synthase (iNOS), Fas, caspase-8 and nitric oxide (NO) in thioglycolate-elicited peritoneal macrophages. SOM caused up-regulation of p53, Bcl-2, Fas and caspase-8 activities, and down-regulation of iNOS expression and NO production. On the other hand, SP slightly induces p53 and highly induces Bcl-2, iNOS expression and NO production. These data suggest that apoptosis by SOM may occur by a Bax- and NO-independent p53 accumulation, and through Fas and caspase-8 activation pathways, and that the inducible expression of Bcl-2 and NO production by SP may contribute to prevent the signals of apoptosis by Bax, and via Fas and caspase-8 activation.
authors.affiliation: Laboratory of Veterinary Anatomy, College of Veterinary Medicine, Chungnam National University, 305-764, Taejeon, South Korea.
authors.forename: B N
authors.initials: BN
authors.lastname: Kang
authors.forename: K S
authors.initials: KS
authors.lastname: Jeong
authors.forename: S J
authors.initials: SJ
authors.lastname: Park
authors.forename: S J
authors.initials: SJ
authors.lastname: Kim
authors.forename: T H
authors.initials: TH
authors.lastname: Kim
authors.forename: H J
authors.initials: HJ
authors.lastname: Kim
authors.forename: S Y
authors.initials: SY
authors.lastname: Ryu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D015153:Blotting, Western; D053181:Caspase 8; D053453:Caspase 9; D020169:Caspases / Q000096:biosynthesis; D002467:Cell Nucleus / Q000648:ultrastructure; D002478:Cells, Cultured; D053938:DNA Fragmentation / Q000187:drug effects; D015536:Down-Regulation; D008262:Macrophage Activation / Q000187:drug effects; D017737:Macrophages, Peritoneal / Q000187:drug effects / Q000276:immunology* / Q000648:ultrastructure; D051379:Mice; D008809:Mice, Inbred C3H; D009569:Nitric Oxide / Q000096:biosynthesis; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis; D013004:Somatostatin / Q000494:pharmacology*; D013373:Substance P / Q000494:pharmacology*; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis; D015854:Up-Regulation; D051028:bcl-2-Associated X Protein; D019014:fas Receptor / Q000096:biosynthesis
chemical_list: C494827:Bax protein, mouse; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53; D051028:bcl-2-Associated X Protein; D019014:fas Receptor; D009569:Nitric Oxide; D013373:Substance P; D013004:Somatostatin; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse; C505526:Casp8 protein, mouse; C506434:Casp9 protein, mouse; D053181:Caspase 8; D053453:Caspase 9; D020169:Caspases