Disease relevance of NANOS2

• RESULTS: Observations of the induction of NOS (iNOS, NOS2) by proinflammatory cytokines led to the hypothesis that nitric oxide (NO) relaxes vascular smooth muscle, thereby producing vasodilation and hypotension in sepsis [1].

High impact information on NANOS2

• Functional redundancy among Nanos proteins and a distinct role of Nanos2 during male germ cell development [2].
• However, salicylate supplement inhibited NOS-2 promoter activities and mRNA and protein levels throughout 24 h [3].
• Cd treatment augmented gene expression of nitric oxide synthase (NOS)1 and NOS2 in the pituitary whereas melatonin decreased it, impairing the activity of Cd [4].
• In mice, the high inducible synthesis of nitric oxide (NO) resulting from inducible NO synthase (iNOS, NOS2) expression by macrophages (Mphi) is considered an essential component of the protective immune response against infection by intracellular pathogens [5].
• On the other hand, using real-time amperometric detection of nitric oxide release shortly after challenge with endomorphins, we showed that only 10(-6) M endomorphin 1 was able to stimulate nitric oxide release from a J774 macrophage cell line by activation of NOS 2 isoenzyme [6].

Biological context of NANOS2

• Objective We analysed several polymorphisms mainly in the promoter region of the inducible NO synthase (NOS2, iNOS) gene and investigated their associations with asthma and/or atopic phenotypes [7].
• In vitro NOS2 expressing TEC had greater resistance to allogeneic lymphocyte-mediated apoptosis [8].
• To address the differences in macrophage function in an animal model, a transgenic mouse was created that contained the entire human NOS2 gene, including the human promoter and all of its exons and introns [9].
• We conclude that NF-kappaB-dependent induction of NOS-2 and macrophage activation must be related to local factor(s) produced in the surroundings of monocytes/macrophages [10].
• Although NOS-2 expression is nuclear factor-kappaB (NF-kappaB)-dependent, no systemic oxidative stress was found, as inferred from the data of plasma TBARS and glutathione disulphide (GSSG) to glutathione (GSH) ratio in circulating blood erythrocytes which remained constant after the acute exercise [10].

Anatomical context of NANOS2

• These genes are differentially expressed in mouse PGCs. nanos2 is predominantly expressed in male germ cells, and the elimination of this gene results in a complete loss of spermatogonia [11].
• These data suggest that endogenous production of NO through renal NOS2 activity can play a protective role in kidney grafts through attenuating Fas-mediated donor cell apoptosis as well as by inhibiting proliferation of inflammatory infiltrating lymphocytes [8].
• Characterization of NO and Cytokine Production in Immune-Activated Microglia and Peritoneal Macrophages Derived from a Mouse Model Expressing the Human NOS2 Gene on a Mouse NOS2 Knockout Background [9].
• Cytokines generate nitric oxide (NO) in osteoblasts and neutrophils through the induction of NO synthase isoforms, endothelial (NOS3) and inducible (NOS2), thereby producing bone loss [12].
• In the cytokine-enriched environment of the chronically rejecting allograft, nitric oxide (NO) is predominantly produced by the inducible isoform of NOS synthase (NOS2) expressed by recipient-derived infiltrating immune cells as well as donor-derived vascular smooth muscle cells and endothelial cells [13].

Associations of NANOS2 with chemical compounds

• As expected, lipopolysaccharide induced de novo NOS 2 transcription within 4 h [6].

Other interactions of NANOS2

• We report the cloning and the functional analyses of nanos2 and nanos3 in mice [11].

Analytical, diagnostic and therapeutic context of NANOS2

• NOS2 (iNOS) deficiency in kidney donor accelerates allograft loss in a murine model [8].

References