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
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