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Abstract
In the heart gap junction intercellular coupling represents the fundament of proper electrical propagation. In cardiac hypertrophy up-regulation of Cx43 has been observed and was suggested as being related to sudden cardiac death. It has been found, that expression and distribution of Cx43, which is the main gap junction forming connexin in the ventricle, is altered in many pathological conditions. We therefore wanted to elucidate whether exposure of cardiomyocytes to chronic pulsatile stretch affects Cx43 and whether mechanotransduction pathways interfere with adrenergic regulation of Cx43, already shown in former experiments.
Highlights
Open AccessMechanotransduction of pulsatile stretch in a cell culture model of cardiac hypertrophy connexin 43 (Cx43) expression
In the heart gap junction intercellular coupling represents the fundament of proper electrical propagation
Neonatal rat cardiomyocytes cultured on gelatine coated Flex Cell cell culture plates were exposed to pulsatile stretch (110% of resting length, 1 Hz) for 24 hours without stimulation of adrenoceptors or in presence of 0,1 μM isoproterenol (Iso) for beta-adrenoceptor stimulation or 0,1 μM phenylephrine (Phe) for alpha1-adrenoceptor stimulation
Summary
Mechanotransduction of pulsatile stretch in a cell culture model of cardiac hypertrophy connexin 43 (Cx43) expression. Address: 1Herzzentrum, Kinderkardiologie, Universität Leipzig, Germany and 2Herzzentrum, Herzchirurgie, Universität Leipzig, Germany * Corresponding author from 12th Joint Meeting of the Signal Transduction Society (STS). Signal Transduction: Receptors, Mediators and Genes Weimar, Germany. Published: 26 February 2009 Cell Communication and Signaling 2009, 7(Suppl 1):A18 doi:10.1186/1478-811X-7-S1-A18. 12th Joint Meeting of the Signal Transduction Society (STS). Signal Transduction: Receptors, Mediators and Genes Frank Entschladen, Karlheinz Friedrich, Ralf Hass and Ottmar Janssen Meeting abstracts – A single PDF containing all abstracts in this Supplement is available here.
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