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Effects on expression profile of acute congestive heart failure (ACHF) patients monocytes by treatment with conventional drugs.

ABSTRACT: Several studies have shown the importance of immune and inflammatory mediators in the pathogenesis of heart failure. In clinical practice has been observed that many conventional drugs can modulate circulating levels of these mediators. Despite, there is poor understanding of the precise mechanisms of these drugs in regulating immune and inflammatory systems. Blood monocytes were isolated from 6 hospitalized patients in Intensive Cardiology Care Unit (ICCU) with symptomatic acute congestive heart failure (ACHF) (NYHA Class III-IV) before and after treatment with conventional drugs (ARBs, ACEIs, diuretics, and beta-blockers). Gene expression analysis (n=11) using whole human genome microarray showed that pharmacological treatment abrogate inflammatory activation of monocytes. The inflammatory response network constructed with Ingenuity Pathway Analysis (IPA) indicates the “TNFR1 signaling” as the most significantly modulated after pharmacological treatment and the pro-inflammatory cytokine TNF-alpha associated with more than a fifth of genes considered.

ORGANISM(S): Homo sapiens

PROVIDER: GSE51888 | GEO | 2013/10/31

SECONDARY ACCESSION(S): PRJNA225678

REPOSITORIES: GEO

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Effects on expression profile of acute congestive heart failure (ACHF) patients monocytes by treatment with conventional drugs.

Project description:Several studies have shown the importance of immune and inflammatory mediators in the pathogenesis of heart failure. In clinical practice has been observed that many conventional drugs can modulate circulating levels of these mediators. Despite, there is poor understanding of the precise mechanisms of these drugs in regulating immune and inflammatory systems. Blood monocytes were isolated from 6 hospitalized patients in Intensive Cardiology Care Unit (ICCU) with symptomatic acute congestive heart failure (ACHF) (NYHA Class III-IV) before and after treatment with conventional drugs (ARBs, ACEIs, diuretics, and beta-blockers). Gene expression analysis (n=11) using whole human genome microarray showed that pharmacological treatment abrogate inflammatory activation of monocytes. The inflammatory response network constructed with Ingenuity Pathway Analysis (IPA) indicates the M-bM-^@M-^\TNFR1 signalingM-bM-^@M-^] as the most significantly modulated after pharmacological treatment and the pro-inflammatory cytokine TNF-alpha associated with more than a fifth of genes considered. In this study, we analyzed the expression profiles of 6 biological replicates of blood monocytes from ACHF patients pre- and post-treatment with conventional drugs (ARBs, ACEIs, diuretics, and beta-blockers). All RNAs from pre-treatment monocytes were hybridized against RNAs from post-treatment RNAs. We performed a total of 11 technical replicates.

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