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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse pressure overload induced cardiomyopathy in gp130 knock-out mice

ABSTRACT: Comparison between wild-type and cardiomyocyte-restricted knock-out of IL6 cytokines receptor component gp130 after surgical intervention for pressure-overload induced cardiomyopathy.

ORGANISM(S): Mus musculus

SUBMITTER: Sylvain Pradervand

PROVIDER: E-MEXP-104 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Nkx2-5 pathways and congenital heart disease; loss of ventricular myocyte lineage specification leads to progressive cardiomyopathy and complete heart block.

Pashmforoush Mohammad M Lu Jonathan T JT Chen Hanying H Amand Tara St TS Kondo Richard R Pradervand Sylvain S Evans Sylvia M SM Clark Bob B Feramisco James R JR Giles Wayne W Ho Siew Yen SY Benson D Woodrow DW Silberbach Michael M Shou Weinian W Chien Kenneth R KR

Cell 20040401 3

Human mutations in Nkx2-5 lead to progressive cardiomyopathy and conduction defects via unknown mechanisms. To define these pathways, we generated mice with a ventricular-restricted knockout of Nkx2-5, which display no structural defects but have progressive complete heart block, and massive trabecular muscle overgrowth found in some patients with Nkx2-5 mutations. At birth, mutant mice display a hypoplastic atrioventricular (AV) node and then develop selective dropout of these conduction cells. ...[more]

PMID: 15109497

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Transcription profiling of mouse pressure overload induced cardiomyopathy time series

Project description:Expression profiles at various time points after surgical intervention for pressure-overload induced cardiac hypertrophy and failure.

2004-06-30 | E-MEXP-105 | biostudies-arrayexpress

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Project description:Determination of gene expression changes in hindlimb muscle (gastrocnemius/soleus) of mdx (dystrophin-deficient) mice at postnatal ages 7, 14, 23, 28, 56, and 112.

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Project description:Gp130 dependent gene expression was analyzed in a previously established hepatocyte-specific gp130-knockout mouse model. Whole transcriptome analysis for isolated hepatocytes was performed to measure tissue specific responses after proinflammatory stimulus with IL-6 across different time points. We observed differences in the hepatocyte-specific transcriptional gp130 dependent response for genes associated with different aspects of the innate immune system. Our findings suggest a complex network of tightly-linked genes involved in the early activation of different parts of the innate immune response including acute phase proteins, complement and coagulation cascade. Total RNA obtained from a total number of 61 samples of isolated hepatocytes of hepatocyte-specific gp130-knockout and gp130flox mice, which were subjected to Il-6 treatment for 0, 1, 3, 6 or 12 hours, respectively.

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Project description:Purpose: Recently discovered activating Interleukin-6 receptor subunit beta (IL6ST, encoding glycoprotein 130 (gp130)) mutations, as well as germline Signal transducer and activator of transcription 3 (STAT3) gain-of-function mutations are associated with multi-organ autoimmunity, severe morbidity, and adverse prognosis, resulting in an unmet medical need. Methods: To dissect crucial cellular subsets and disease biology involved in activated gp130 signaling, in this study we constitutively activated the gp130/JAK/STAT3 axis by means of a transgene, L-gp130, specifically targeted to T-cells. Results: Activating gp130 signaling in vivo resulted in fatal early-onset multi-organ autoimmunity, resembling numerous clinical features of human STAT3 gain-of-function disease. We observed strong T-cell activation and effector differentiation, accompanied by TH17 expansion and interferon-gamma production. Transcriptome profiling of murine CD4+ and CD8+ T-cells revealed commonly dysregulated genes and a STAT3 gain-of-function signature that was used to discriminate between STAT3 gain-of-function and healthy control patients. Conclusions: Hyperactive gp130/STAT3 signaling leads to strong TH17-mediated autoimmunity phenotypically resembling human STAT3 gain-of-function disease and identify TH17-cells as a key cellular subset for initiation and maintenance of autoimmunity

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