More severe cellular phenotype in human idiopathic dilated cardiomyopathy compared to ischemic heart disease

Nazha Hamdani, A. Borbély, Sophie P G R Veenstra, Viola Kooij, Wim Vrydag, Ruud Zaremba, Cris Dos Remedios, Hans W M Niessen, Martin C. Michel, Walter J. Paulus, Ger J M Stienen, Jolanda Van Der Velden

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

Activation of the β-adrenergic receptor (βAR) pathway is the main mechanism of the heart to increase cardiac output via protein kinase A (PKA)-mediated phosphorylation of cellular target proteins, and perturbations therein may contribute to cardiac dysfunction in heart failure. In the present study a comprehensive analysis was made of mediators of the βAR pathway, myofilament properties and cardiac structure in patients with idiopathic (IDCM; n = 13) and ischemic (ISHD; n = 10) cardiomyopathy in comparison to non-failing hearts (donor; n = 10) for the following parameters: βAR density, G-coupled receptor kinases 2 and 5, stimulatory and inhibitory G-proteins, phosphorylation of myofilament targets of PKA, protein phosphatase 1, phospholamban, SERCA2a and single myocyte contractility. All parameters exhibited the expected alterations of heart failure, but for most of them the extent of alteration was greater in IDCM than in ISHD. Histological analysis also revealed higher collagen in IDCM compared to ISHD. Alterations in the βAR pathway are more pronounced in IDCM than in ISHD and may reflect sequential changes in cellular protein composition and function. Our data indicate that cellular dysfunction is more severe in IDCM than in ISHD.

Original languageEnglish
Pages (from-to)289-301
Number of pages13
JournalJournal of Muscle Research and Cell Motility
Volume31
Issue number4
DOIs
Publication statusPublished - Dec 2010

Fingerprint

Dilated Cardiomyopathy
Adrenergic Receptors
Myocardial Ischemia
Phenotype
Phosphorylation
Myofibrils
Cyclic AMP-Dependent Protein Kinases
Heart Failure
Protein Phosphatase 1
Cardiomyopathies
GTP-Binding Proteins
Cardiac Output
Muscle Cells
Proteins
Phosphotransferases
Collagen
Chemical activation
Tissue Donors
Chemical analysis

Keywords

  • β-Adrenergic receptor
  • Cardiomyocyte
  • Collagen
  • Myofilament function
  • Protein phosphorylation

ASJC Scopus subject areas

  • Physiology
  • Cell Biology
  • Biochemistry

Cite this

More severe cellular phenotype in human idiopathic dilated cardiomyopathy compared to ischemic heart disease. / Hamdani, Nazha; Borbély, A.; Veenstra, Sophie P G R; Kooij, Viola; Vrydag, Wim; Zaremba, Ruud; Dos Remedios, Cris; Niessen, Hans W M; Michel, Martin C.; Paulus, Walter J.; Stienen, Ger J M; Van Der Velden, Jolanda.

In: Journal of Muscle Research and Cell Motility, Vol. 31, No. 4, 12.2010, p. 289-301.

Research output: Contribution to journalArticle

Hamdani, N, Borbély, A, Veenstra, SPGR, Kooij, V, Vrydag, W, Zaremba, R, Dos Remedios, C, Niessen, HWM, Michel, MC, Paulus, WJ, Stienen, GJM & Van Der Velden, J 2010, 'More severe cellular phenotype in human idiopathic dilated cardiomyopathy compared to ischemic heart disease', Journal of Muscle Research and Cell Motility, vol. 31, no. 4, pp. 289-301. https://doi.org/10.1007/s10974-010-9231-8
Hamdani, Nazha ; Borbély, A. ; Veenstra, Sophie P G R ; Kooij, Viola ; Vrydag, Wim ; Zaremba, Ruud ; Dos Remedios, Cris ; Niessen, Hans W M ; Michel, Martin C. ; Paulus, Walter J. ; Stienen, Ger J M ; Van Der Velden, Jolanda. / More severe cellular phenotype in human idiopathic dilated cardiomyopathy compared to ischemic heart disease. In: Journal of Muscle Research and Cell Motility. 2010 ; Vol. 31, No. 4. pp. 289-301.
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