Cyclical stretch induces structural changes in atrial myocytes
Autor: | Alexander H. Maass, Wiek H. van Gilst, Anne Margreet De Jong, Rudolf A. de Boer, Isabelle C. Van Gelder, Silke U. Oberdorf-Maass |
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Přispěvatelé: | Cardiovascular Centre (CVC) |
Jazyk: | angličtina |
Rok vydání: | 2013 |
Předmět: |
Potassium Channels
MATRIX METALLOPROTEINASES CARDIAC GENE-EXPRESSION p38 Mitogen-Activated Protein Kinases CARDIOMYOCYTES Muscle hypertrophy Rats Sprague-Dawley Atrial natriuretic peptide Atrial Fibrillation Natriuretic Peptide Brain Atria Myocytes Cardiac remodelling Extracellular Signal-Regulated MAP Kinases Pravastatin Cell Death Anticholesteremic Agents Calcineurin OVINE MODEL Gene Expression Regulation Developmental Brain natriuretic peptide Potassium channel Molecular Medicine HEART-FAILURE FIBRILLATION medicine.symptom stretch Atrial Natriuretic Factor Signal Transduction medicine.medical_specialty Programmed cell death Growth Differentiation Factor 15 Atrial Pressure Biology CALCIUM Internal medicine Pressure medicine Animals Heart Atria Fibrillation cell culture RAT HEARTS Atrial Remodeling Original Articles Cell Biology MITRAL REGURGITATION Actins Rats Endocrinology Animals Newborn Stress Mechanical MECHANICAL STRETCH |
Zdroj: | Journal of Cellular and Molecular Medicine Journal of cellular and molecular medicine, 17(6), 743-753. Wiley |
ISSN: | 1582-1838 |
Popis: | Atrial fibrillation (AF) often occurs in the presence of an underlying disease. These underlying diseases cause atrial remodelling, which make the atria more susceptible to AF. Stretch is an important mediator in the remodelling process. The aim of this study was to develop an atrial cell culture model mimicking remodelling due to atrial pressure overload. Neonatal rat atrial cardiomyocytes (NRAM) were cultured and subjected to cyclical stretch on elastic membranes. Stretching with 1Hz and 15% elongation for 30min. resulted in increased expression of immediate early genes and phosphorylation of Erk and p38. A 24-hr stretch period resulted in hypertrophy-related changes including increased cell diameter, reinduction of the foetal gene program and cell death. No evidence of apoptosis was observed. Expression of atrial natriuretic peptide, brain natriuretic peptide and growth differentiation factor-15 was increased, and calcineurin signalling was activated. Expression of several potassium channels was decreased, suggesting electrical remodelling. Atrial stretch-induced change in skeletal -actin expression was inhibited by pravastatin, but not by eplerenone or losartan. Stretch of NRAM results in elevation of stress markers, changes related to hypertrophy and dedifferentiation, electrical remodelling and cell death. This model can contribute to investigating the mechanisms involved in the remodelling process caused by stretch and to the testing of pharmaceutical agents. |
Databáze: | OpenAIRE |
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