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

  • 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
Original Contribution

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.

Keywords

Heart failure Transverse aortic constriction Gene expression Genetic background Cardiac function 

Notes

Acknowledgements

We thank Dr. Dietmar Pfeifer at the University of Freiburg for technical assistance in performing microarray analyses.

Funding

This study was supported by a research grant of the Deutsche Forschungsgemeinschaft to H.B. (Bu2126/3-1), and by a National Institutes of Health (NIH) grant to A.R.W. (HL133011). Training support was provided by NIH T32 to M.E.P. (T32HD071866).

Compliance with ethical standards

Conflict of interest

The authors declare that they have no conflict of interest.

Supplementary material

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Copyright information

© Springer-Verlag GmbH Germany, part of Springer Nature 2017

Authors and Affiliations

  • Christoph Koentges
    • 1
  • Mark E. Pepin
    • 2
  • Carolyn Müsse
    • 1
  • Katharina Pfeil
    • 1
  • Sonia V. Viteri Alvarez
    • 1
  • Natalie Hoppe
    • 1
  • Michael M. Hoffmann
    • 3
    • 4
  • Katja E. Odening
    • 1
    • 3
  • Samuel Sossalla
    • 5
  • Andreas Zirlik
    • 1
    • 3
  • Lutz Hein
    • 3
    • 6
  • Christoph Bode
    • 1
    • 3
  • Adam R. Wende
    • 2
  • Heiko Bugger
    • 1
    • 3
  1. 1.Cardiology and Angiology I, Heart CenterFreiburg UniversityFreiburgGermany
  2. 2.Division of Molecular and Cellular Pathology, Department of PathologyUniversity of Alabama at BirminghamBirminghamUSA
  3. 3.Faculty of MedicineUniversity of FreiburgFreiburgGermany
  4. 4.Institute for Clinical Chemistry and Laboratory Medicine, Medical CenterUniversity of FreiburgFreiburgGermany
  5. 5.Department of Internal Medicine IIUniversity Hospital RegensburgRegensburgGermany
  6. 6.Institute of Experimental and Clinical Pharmacology, BIOSS Center for Biological Signaling StudiesUniversity of FreiburgFreiburgGermany

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