C2c12 Skeletal Muscle Cells Adopt Cardiac-like Sodium Current Properties in a Cardiac Cell Environment.
From: Center of Biomolecular Medicine and Pharmacology, Institute of Pharmacology, Medical Univ. of Vienna, Waehringerstrasse 13A, A-1090 Vienna, Austria.
American journal of physiology. Heart and circulatory physiology
- Publish Date: Jan 2007
- ISSN: 0363-6135
- Volume: 292
- Issue: 1
- Pages: H439-50
- Medium: Print
- Language: English
- Citation (JAMA): Zebedin Eva, Mille Markus, Speiser Maria, et al. C2c12 Skeletal Muscle Cells Adopt Cardiac-like Sodium Current Properties in a Cardiac Cell Environment.. Am. J. Physiol. Heart Circ. Physiol. Jan 2007;292:H439-50
Abstract
Intracardiac transplantation of undifferentiated skeletal muscle cells (myoblasts) has emerged as a promising therapy for myocardial infarct repair and is already undergoing clinical trials. The fact that cells originating from skeletal muscle have different electrophysiological properties than cardiomyocytes, however, may considerably limit the success of this therapy and, in addition, cause side effects. Indeed, a major problem observed after myoblast transplantation is the occurrence of ventricular arrhythmias. The most often transient nature of these arrhythmias may suggest that, once transplanted into cardiac tissue, skeletal muscle cells adopt more cardiac-like electrophysiological properties. To test whether a cardiac cell environment can indeed modify electrophysiological parameters of skeletal muscle cells, we treated mouse C(2)C(12) myocytes with medium preconditioned by primary cardiocytes and compared their functional sodium current properties with those of control cells. We found this treatment to significantly alter the activation and inactivation properties of sodium currents from “skeletal muscle” to more “cardiac”-like ones. Sodium currents of cardiac-conditioned cells showed a reduced sensitivity to block by tetrodotoxin. These findings and reverse transcription PCR experiments suggest that an upregulation of the expression of the cardiac sodium channel isoform Na(v)1.5 versus the skeletal muscle isoform Na(v)1.4 is responsible for the observed changes in sodium current function. We conclude that cardiomyocytes alter sodium channel isoform expression of skeletal muscle cells via a paracrine mechanism. Thereby, skeletal muscle cells with more cardiac-like sodium current properties are generated.
Mesh Headings (Keywords): Animals, Animals, Newborn, Cell Differentiation, Cell Line, Cells, Cultured, Coculture Techniques, Ion Channel Gating, Mice, Myoblasts, Skeletal, Myocytes, Cardiac, Paracrine Communication, Rats, Rats, Wistar, Sodium Channels
Check for Full Text / PubMed Unique Identifier (PMID): 16980339
This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.
Linked medical terms appearing on this page are added by Healia to help readers find more information and are not part of the original PubMed document.
The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.