IMR Press / FBE / Volume 5 / Issue 3 / DOI: 10.2741/E667

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.


Stretch-induced phosphorylation of MAPK and p90RSK in human myocardium

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1 Division of Cardiology, Medical University of Graz, Graz, Austria
2 Department of Internal Medicine and Cardiology, University Hospital of Marburg and Giessen, Philipps-University of Marburg, Marburg, Germany
3 Working Group of Cardiac Metabolism, Medical University of Graz, Graz, Austria
4 Department of Cardiology and Pneumology, University Medicine Goettingen, Goettingen, Germany
5 Institute of Pharmacology and Clinical Pharmacy, Philipps-University of Marburg, Marburg, Germany

*Author to whom correspondence should be addressed.


Front. Biosci. (Elite Ed) 2013, 5(3), 883–892;
Published: 1 June 2013

Stretch activates various signal transduction pathways including mitogen-activated protein kinases (MAPK). Stretch-induced phosphorylation of MAPKcontribution to contractility in human myocardium is unknown. We tested the effects of stretch on p44/42-, p38-MAPK and p90rsk phosphorylation and the functional relevance for force development in failing (F) and nonfailing (NF) human myocardium. Trabeculae were stretched to a diastolic tension of 12mN/mm2 for 2.5 to 30 minutes and frozen for Western Blot analysis. Stretch induced a time-dependent increase in phosphorylation of p44/42-, p38-MAPK and p90rsk. For functional analysis, trabeculae from F myocardium were stretched and the immediate (Frank-Starling mechanism; FSM) and delayed (slow force response; SFR) increase in twitch force was assessed before and after blocking the activation of p44/42- MAPK (30 mol/L U0126) and p38-MAPK (10 mol/L SB203580). Inhibition of p44/42-MAPK almost completely blocked the SFR (106.7±3.7% vs. 125.4±2.9%), while p38- MAPK-blockade significantly increased the SFR (124.6±1.9% vs. 121.2±2.2%). Stretch induced a timedependent increase in p44/42-, p38-MAPK and p90rsk phosphorylation in F and NF myocardium. While p44/42- MAPK phosphorylation contributed to the SFR, p38- MAPK activation antagonized the stretch-induced SFR.

Human Myocardium
Slow Force Response
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