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01.01.2018 | Original Contribution

Gene expression analysis to identify mechanisms underlying heart failure susceptibility in mice and humans

verfasst von: Christoph Koentges, Mark E. Pepin, Carolyn Müsse, Katharina Pfeil, Sonia V. Viteri Alvarez, Natalie Hoppe, Michael M. Hoffmann, Katja E. Odening, Samuel Sossalla, Andreas Zirlik, Lutz Hein, Christoph Bode, Adam R. Wende, Heiko Bugger

Erschienen in: Basic Research in Cardiology | Ausgabe 1/2018

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Abstract

Genetic factors are known to modulate cardiac susceptibility to ventricular hypertrophy and failure. To determine how strain influences the transcriptional response to pressure overload-induced heart failure (HF) and which of these changes accurately reflect the human disease, we analyzed the myocardial transcriptional profile of mouse strains with high (C57BL/6J) and low (129S1/SvImJ) susceptibility for HF development, which we compared to that of human failing hearts. Following transverse aortic constriction (TAC), C57BL/6J mice developed overt HF while 129S1/SvImJ did not. Despite a milder aortic constriction, impairment of ejection fraction and ventricular remodeling (dilation, fibrosis) was more pronounced in C57BL/6J mice. Similarly, changes in myocardial gene expression were more robust in C57BL/6J (461 genes) compared to 129S1/SvImJ mice (71 genes). When comparing these patterns to human dilated cardiomyopathy (1344 genes), C57BL/6J mice tightly grouped to human hearts. Overlay and bioinformatic analysis of the transcriptional profiles of C57BL/6J mice and human failing hearts identified six co-regulated genes (POSTN, CTGF, FN1, LOX, NOX4, TGFB2) with established link to HF development. Pathway enrichment analysis identified angiotensin and IGF-1 signaling as most enriched putative upstream regulator and pathway, respectively, shared between TAC-induced HF in C57BL/6J mice and in human failing hearts. TAC-induced heart failure in C57BL/6J mice more closely reflects the gene expression pattern of human dilated cardiomyopathy compared to 129S1/SvImJ mice. Unbiased as well as targeted gene expression and pathway analyses identified periostin, angiotensin signaling, and IGF-1 signaling as potential causes of increased HF susceptibility in C57BL/6J mice and as potentially useful drug targets for HF treatment.

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Titel: Gene expression analysis to identify mechanisms underlying heart failure susceptibility in mice and humans
verfasst von: Christoph Koentges
Mark E. Pepin
Carolyn Müsse
Katharina Pfeil
Sonia V. Viteri Alvarez
Natalie Hoppe
Michael M. Hoffmann
Katja E. Odening
Samuel Sossalla
Andreas Zirlik
Lutz Hein
Christoph Bode
Adam R. Wende
Heiko Bugger
Publikationsdatum: 01.01.2018
Verlag: Springer Berlin Heidelberg
Erschienen in: Basic Research in Cardiology / Ausgabe 1/2018
Print ISSN: 0300-8428
Elektronische ISSN: 1435-1803
DOI: https://doi.org/10.1007/s00395-017-0666-6

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STAT3 as a common signal of ischemic conditioning: a lesson on “rigor and reproducibility” in preclinical studies on cardioprotection

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Periostin in cardiovascular disease and development: a tale of two distinct roles

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Springer Medizin

Gene expression analysis to identify mechanisms underlying heart failure susceptibility in mice and humans

Abstract

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STAT3 as a common signal of ischemic conditioning: a lesson on “rigor and reproducibility” in preclinical studies on cardioprotection

Periostin in cardiovascular disease and development: a tale of two distinct roles

Kompaktes Leitlinien-Wissen Innere Medizin (Link öffnet in neuem Fenster)

Neu im Fachgebiet Kardiologie

Schützen GLP1-Rezeptor-Agonisten vor kardiovaskulären Komplikationen nach Pneumonie?

Beeinträchtigte Ventrikelfüllung erhöht die COPD-Mortalität

Auf dem Weg zur Präzisionsmedizin in der Kardiologie

Nach kardiovaskulärer Erkrankung steigt das Krebsrisiko

EKG Essentials: EKG befunden mit System (Link öffnet in neuem Fenster)

Update Kardiologie

Springer Medizin

Abstract

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