Modulation of cardiac contractility by serine/threonine protein phosphatase type 5

Ulrich Gergs, Peter Boknik, Igor B Buchwalow, Larissa Fabritz, Nicole Gründker, Dana Kucerova, Marek Matus, Franziska Werner, Wilhelm Schmitz, Joachim Neumann

Research output: Contribution to journalArticlepeer-review

8 Citations (Scopus)


BACKGROUND: Protein phosphatase 5 (PP5) a serine/threonine phosphatase is ubiquitously expressed in mammalian tissues including the heart, but its physiological role in the heart is still unknown. Therefore, we used a transgenic mouse model to get a first insight into the cardiac role of PP5.

METHODS AND RESULTS: We generated transgenic mice with cardiac myocyte specific overexpression of PP5. Successful overexpression of PP5 was demonstrated by Western blotting, immunohistochemistry and enhanced arachidonic acid-stimulated protein phosphatase activity in transgenic hearts. Cardiac function was examined on the level of isolated cardiac myocytes, isolated organs and in intact animals. Whereas Ca(2+) transients and cell shortening remained unchanged, L-type Ca(2+) currents were decreased in isolated cardiac myocytes from transgenic mice. Ventricular contractility was reduced in isolated perfused hearts under basal conditions and after β-adrenergic stimulation. In intact animals, echocardiography revealed increased left ventricular diameters and decreased contractility and invasively measured hemodynamic performance by left ventricular catheterization demonstrated a reduced response to β-adrenergic stimulation in transgenic mice compared to wild type.

CONCLUSIONS: Overexpression of PP5 affected contractility and β-adrenergic signaling in the hearts of transgenic mice. Taken together, these findings are indicative of a regulatory role of PP5 in cardiac function.

Original languageEnglish
Pages (from-to)116-21
Number of pages6
JournalInternational Journal of Cardiology
Issue number2
Publication statusPublished - 26 Jan 2012


  • Animals
  • Calcium Channels, L-Type
  • Gene Expression Regulation, Enzymologic
  • Humans
  • Mice
  • Mice, Transgenic
  • Myocardial Contraction
  • Myocytes, Cardiac
  • Nuclear Proteins
  • Patch-Clamp Techniques
  • Phosphoprotein Phosphatases
  • Rats
  • Receptors, Adrenergic, beta
  • Signal Transduction
  • Transgenes


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