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Transcription profiling of mouse autoimmune and diabetic NOF animals reveals the curative and beta cell regenerative effects of alpha1 antitrypsin treatment

ABSTRACT: In this study, we performed the gene expression analysis of the Normal, Diabetic and AAT treated NOD mice to elucidate the transcriptional changes induced by AAT. This will assist in identifying the biological processes / pathways involved in curative mechanism of AAT. Experiment Overall Design: Duplicate samples of Normal, Diabetic and AAT treated NOD mice were analyzed.

ORGANISM(S): Mus musculus

SUBMITTER: Terry Strom

PROVIDER: E-GEOD-10478 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Curative and beta cell regenerative effects of alpha1 antitrypsin treatment in autoimmune diabetic NOD mice

Project description:In this study, we performed the gene expression analysis of the Normal, Diabetic and AAT treated NOD mice to elucidate the transcriptional changes induced by AAT. This will assist in identifying the biological processes / pathways involved in curative mechanism of AAT. Keywords: alpha1 antitrypsin treatment

2008-12-31 | GSE10478 | GEO

Curative and beta cell regenerative effects of alpha1-antitrypsin treatment in autoimmune diabetic NOD mice.

Project description:Invasive insulitis is a destructive T cell-dependent autoimmune process directed against insulin-producing beta cells that is central to the pathogenesis of type 1 diabetes mellitus (T1DM) in humans and the clinically relevant nonobese diabetic (NOD) mouse model. Few therapies have succeeded in restoring long-term, drug-free euglycemia and immune tolerance to beta cells in overtly diabetic NOD mice, and none have demonstrably enabled enlargement of the functional beta cell mass. Recent studies have emphasized the impact of inflammatory cytokines on the commitment of antigen-activated T cells to various effector or regulatory T cell phenotypes and insulin resistance and defective insulin signaling. Hence, we tested the hypothesis that inflammatory mechanisms trigger insulitis, insulin resistance, faulty insulin signaling, and the loss of immune tolerance to islets. We demonstrate that treatment with alpha1-antitrypsin (AAT), an agent that dampens inflammation, does not directly inhibit T cell activation, ablates invasive insulitis, and restores euglycemia, immune tolerance to beta cells, normal insulin signaling, and insulin responsiveness in NOD mice with recent-onset T1DM through favorable changes in the inflammation milieu. Indeed, the functional mass of beta cells expands in AAT-treated diabetic NOD mice.

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The role for TNF-alpha in murine type 1 and 2 diabetes

Project description:To search for new therapeutic targets for type 1 & 2 diabetes, we have applied genome wide transcriptional profiling and systems biology oriented bioinformatics analysis to examine the impact of the Power mix(PM) and Alpha-1 Anti-Trypsin( AAT) regimens upon pancreatic lymph node (PLN) and fat, a crucial tissue for insulin dependent glucose disposal, in new onset diabetic NOD mice. Transcriptional profiles of fat and PLNs in normal (non diabetic) NOD mice (NOR), new onset diabetic (DIA), new onset diabetic NOD mice treated with AAT or PM were perfromed in this study

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Candida albicans: control vs. alpha1-antitrypsin (AAT) treatment

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Genomic profiling of type-1 adult diabetic and aged normoglycemic mice liver

Project description:Here we characterized and compared differential gene expression from diabetic and normoglycemic NOD mice and from aged and young-adults Balb/c mice. Total RNA from NOD diabetic (3 weeks with glicemia over 500mg/dl) and normoglycemic NOD mice from the same age was used. To compare the effects of aging in genomic expression, total RNA from young-adult Balb/c (9 weeks old) and middle-aged Balb/c (47 weeks old) were used.

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Alpha-1-antitrypsin binds to the glucocorticoid receptor with anti-inflammatory and anti-mycobacterial significance in macrophages

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2012-11-22 | GSE33891 | GEO

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