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Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mice heart tissue treated with tetrahydrobiopterin compounds

ABSTRACT: Tetrahydrobiopterin compounds prolong allograft survival independent of their effect on nitric oxide synthase activity

ORGANISM(S): Mus musculus

SUBMITTER: Oliver Alexander Wrulich

PROVIDER: E-GEOD-1809 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Tetrahydrobiopterin compounds prolong allograft survival independently of their effect on nitric oxide synthase activity.

Brandacher Gerald G Maglione Manuel M Schneeberger Stefan S Obrist Peter P Thoeni Guntram G Wrulich Oliver A OA Werner-Felmayer Gabriele G Margreiter Raimund R Werner Ernst R ER

Transplantation 20060201 4

<h4>Background</h4>In previous work, the four-amino analogue of tetrahydrobiopterin, a novel, selective inhibitor of inducible nitric oxide synthase, has been shown to prolong survival of murine cardiac allografts.<h4>Methods</h4>To further elucidate the underlying molecular immunosuppressive mechanism, we compared the effect of four-amino tetrahydrobiopterin with that of the unsubstituted parent compound tetrahydrobiopterin and of N-(iminoethyl)-L-lysine (L-NIL), a nonpterin inhibitor of induci ...[more]

PMID: 16495807

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Cardiac grafts pteridine cyclosporinA and NIL treated

Project description:Tetrahydrobiopterin compounds prolong allograft survival independent of their effect on nitric oxide synthase activity Keywords: other

2005-02-28 | GSE1809 | GEO

IFN-M-NM-3-induced iNOS expression in regulatory macrophages prolongs allograft graft survival in fully immunocompetent recipients.

Project description:Mouse monocytes exposed to M-CSF and IFN-M-NM-3 were driven to a suppressor phenotype over a seven day culture period. The resulting regulatory macrophages (M regs) expressed markers distinguishing them from M0-, M1-, and M2-polarised macrophages and monocyte-derived DCs. M regs completely suppressed polyclonal T cell proliferation through an inducibile nitric oxide synthase (iNOS)-dependent mechanism. Additionally, M regs were found to eliminate cocultured T cells in an allospecific fashion. In a heterotopic heart transplant model, a single intravenous administration of 5x10^6 donor-strain M regs prior to transplantation significantly prolonged allograft survival in fully immunocompetent recipients using both the stringent C3H-to-BALB/c and C57BL/6-to-BALB/c strain combinations; this graft-protective effect was alloantigen-specific. M regs from Nos2-deficient mice did not prolong allograft survival, proving that M reg function in vivo is iNOS-mediated and dependent on living cells. Co-treatment with 1 mg/kg/day rapamycin for 10 days post-transplant markedly enhanced the effect of M regs. In untransplanted C57BL/6 recipients, M regs of BALB/c origin were detectable for up to 2 weeks post-infusion. It is concluded that mouse M regs represent a novel, phenotypically distinct subset of tolerogenic macrophages, which resemble human M regs in their derivation, phenotype and in vitro functions. The dataset comprises 36 samples divided into twelve sample groups each representing a certain monocyte/macrophage subtype

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The alterations of gene expression in aorta from endothelial nitric oxide synthase (eNOS)-deficient mice

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Expression data from murine colon tissue after exposure to 4% DSS for 6 days DSS followed by 4 days of water or 1% L-arginine

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S-nitrosylation in zebra fish tissue regeneration

Project description:we found that inducible nitric oxide synthase (iNOS) is critical to this process by virtue of its ability to induce post-translational S-nitrosylation of epigenetic enzymes. The possible link between induction of PSC, S-nitrosylation and tissue regeneration remains largely unexplored. Here, we show that the inducible NO synthase (iNOS) translocates from the cytoplasm to the nucleus during regeneration of the zebrafish tailfin and that this is associated with alterations in the nuclear S-nitrosylome.

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