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Real-time quantitative PCR analysis of mice lung tissue [S100A8 time course]

ABSTRACT: Recombinant-murine S100A8 were used at 10 mg/50 ml in Hanks Balanced Salt solution (HBSS) or control HBSS administered onto the nares of BALB/C mice. To assess direct effects, mice were sacrificed 1, 4, 6, or 12 h post-inhalation of S100A8. Because S100A8 is reported to initiate proinflammatory responses by ligating TLR4 and/or RAGE, a quantitative PCR array was developed to analyze 49 genes, selected to reflect potential acute inflammatory changes induced by ligation of these receptors.

ORGANISM(S): Mus musculus

PROVIDER: GSE74122 | GEO | 2016/08/01

SECONDARY ACCESSION(S): PRJNA299111

REPOSITORIES: GEO

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Real-time quantitative PCR analysis of mice lung tissue [S100A8 time course]

Project description:Recombinant-murine S100A8 were used at 10 mg/50 ml in Hanks Balanced Salt solution (HBSS) or control HBSS administered onto the nares of BALB/C mice. To assess direct effects, mice were sacrificed 1, 4, 6, or 12 h post-inhalation of S100A8. Because S100A8 is reported to initiate proinflammatory responses by ligating TLR4 and/or RAGE, a quantitative PCR array was developed to analyze 49 genes, selected to reflect potential acute inflammatory changes induced by ligation of these receptors. Expression of inflammatory genes was evaluated with the RT-qPCR array. Relative quantities of mRNA in duplicate samples were obtained using the LightCyclerÂ® 480 Software 1.5 and the Efficiency-Method.

2016-08-01 | E-GEOD-74122 | biostudies-arrayexpress

Real-time quantitative PCR analysis of mice lung tissue [S100A9 time course]

Project description:Recombinant-murine S100A9 were used at 10 mg/50 ml in Hanks Balanced Salt solution (HBSS) or control HBSS administered onto the nares of BALB/C mice. To assess direct effects, mice were sacrificed 1, 4, 6, or 12 h post-inhalation of S100A9. Because S100A9 is reported to initiate proinflammatory responses by ligating TLR4 and/or RAGE, a quantitative PCR array was developed to analyze 49 genes, selected to reflect potential acute inflammatory changes induced by ligation of these receptors.

2016-08-01 | GSE74128 | GEO

Real-time quantitative PCR analysis of mice lung tissue (2)

Project description:Recombinant-murine S100A8 and the corresponding Cys42 to Ala42 mutant were used at 10 mg/50 ml HBSS administered onto the nares of BALB/C mice. To assess direct effects, mice were sacrificed 1, 4, 6, 12 or 20 h post-inhalation of S100A8 or 12 and 20 h post-inhalation of Ala42S100A8. For comparison with Dex inhalation (used at 10 mg/50 ml HBSS), lungs were harvested 6 and 12 h post administration. Because S100A8 is reported to initiate proinflammatory responses by ligating TLR4 and/or RAGE, a quantitative PCR array was developed to analyse 63 genes, selected to reflect potential acute inflammatory changes induced by ligation of these receptors.

2013-11-26 | GSE52719 | GEO

Real-time quantitative PCR analysis of mice lung tissue (1)

2013-11-26 | GSE52718 | GEO

Real-time quantitative PCR analysis of mice lung tissue (1)

2013-11-26 | E-GEOD-52718 | biostudies-arrayexpress

Real-time quantitative PCR analysis of mice lung tissue (2)

2013-11-26 | E-GEOD-52719 | biostudies-arrayexpress

Real-time quantitative PCR analysis of mice lung tissue [S100A9 time course]

2016-08-01 | E-GEOD-74128 | biostudies-arrayexpress

Real-time quantitative PCR analysis of mice lung tissue after inhalation of S100A8, S100A8 dimer, S100A9 or S100A8/A9 complex in acute lung [S100A8S100A9 LPS induced ALI]

Project description:LPS (10 μg/50 μl PBS; E. coli Serotype 055:B5, Sigma-Aldrich) was administered onto the nares. Baseline levels of genes in mice treated with vehicle (Hanks Balanced Salt solution (HBSS) and PBS), Intranasal S100s (10 μg/50 μl HBSS) were given 2 h before LPS; control mice received equal volumes of PBS and HBSS. Mice were sacrificed 4 h post LPS inhalation.

2016-08-01 | GSE74127 | GEO

Real-time quantitative PCR analysis of mice lung tissue after inhalation of S100A8, S100A8 dimer, S100A9 or S100A8/A9 complex in acute lung [S100A8S100A9 LPS induced ALI]

Project description:LPS (10 Î¼g/50 Î¼l PBS; E. coli Serotype 055:B5, Sigma-Aldrich) was administered onto the nares. Baseline levels of genes in mice treated with vehicle (Hanks Balanced Salt solution (HBSS) and PBS), Intranasal S100s (10 Î¼g/50 Î¼l HBSS) were given 2 h before LPS; control mice received equal volumes of PBS and HBSS. Mice were sacrificed 4 h post LPS inhalation. Expression of inflammatory genes was evaluated with the RT-qPCR array. Relative quantities of mRNA in duplicate samples were obtained using the LightCyclerÂ® 480 Software 1.5 and the Efficiency-Method.

2016-08-01 | E-GEOD-74127 | biostudies-arrayexpress

Elevated levels of S100A8 and S100A9 exacerbate muscle mitochondrial fragmentation in sepsis-induced muscle atrophy

Project description:Sepsis-induced skeletal muscle atrophy is common in septic patients with the increases risk of mortality and is associated with myocellular mitochondrial dysfunction. Nevertheless, the specific mechanism of sepsis muscle atrophy remains unclear. Here we conducted a clinical retrospective analysis and observed the elevation of skeletal muscle index (ΔSMI) was an independent risk factor for 60-day mortality in septic patients. Moreover, in mouse model of sepsis, the skeletal muscle atrophy was also observed, which was associated with the upregulation of S100a8/a9-mediated mitochondrial dysfunction. Inhibition of S100a8/a9 significantly improved mitochondrial function and alleviated muscle atrophy. Conversely, administration of recombinant S100a8/a9 protein exacerbated mitochondrial energy exhaustion and myocyte atrophy. Mechanistically, S100a8/a9 binding to RAGE induced Drp1 phosphorylation and mitochondrial fragmentation, resulting in muscle atrophy. Additionally, RAGE ablation or administration of Drp1 inhibitor significantly reduced Drp1-mediated mitochondrial fission, improved mitochondrial morphology and function. Our findings indicated the pivotal role of S100a8/a9 in driving the mitochondrial fragmentation in septic muscle atrophy. Targeting S100a8/a9-RAGE-initiated mitochondrial fission might offer a promising therapeutic intervention against septic muscle atrophy. Taken together, our data provide a potential mechanism for sepsis-induced muscle atrophy.

2025-01-15 | GSE285318 | GEO

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