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Analysis of the energetic state of heart cells after adenovirus-mediated expression of hALC-1

Item Type:Article
Title:Analysis of the energetic state of heart cells after adenovirus-mediated expression of hALC-1
Creators Name:Zacharzowsky, U.B. and Wolff, G. and Kott, M. and Haase, H. and Bartsch, H. and Nuessler, A.K. and Baltas, L.G. and Karawajew, L. and Morano, I.
Abstract:Expression of the human atrial myosin light chain 1 (hALC-1) in the cardiac ventricle in vivo as well as in primary cultivated adult cardiomyocytes caused a pronounced positive inotropic effect. Therefore, it is one of the most promising candidate gene to treat congestive heart failure (CHF). In this work, we investigated, whether hALC-1 expression also modifies the energetic state of cardiomyocytes. Primary cultivated neonatal rat hearts cells (NRHC) were infected with adenoviral vectors (Ad vectors) containing a hALC-1 cDNA (AdCMV.hALC-1) or a control Ad vector. Infection efficiency of NRHC reached 100% at 50 multiplicity of infection (MOI). Interestingly and in contrast to primary cultures of liver cells, there were no cytotoxic side effects or induction of apoptosis up to MOI 50 in Ad vector infected NRHC. NRHC expressed large amounts of hALC-1 upon infection with AdCMV.hALC-1 which could easily been detected by protein staining and Western blot analysis. Analysis of intracellular hALC-1 localization by double-labeling immunofluorescence of AdCMV.hALC-1 infected cardiomyocytes revealed the typical myofibrillar striation pattern, as well as co-localization of hALC-1 with myosin heavy chains. There was no difference in the oxygen consumption between controls and AdCMV.hALC-1 infected NRHC. These data suggest that first: adenoviral vectors could be used as a safe and effective tool for gene transfer to cardiomyocytes, and second: that a positive inotropic effect of hALC-1 is not associated with enhanced oxygen consumption.
Keywords:Adenovirus, Cardiomyocytes, Gene Transfer, Human ALC-1, Animals, Rats
Source:Journal of Cellular Biochemistry
ISSN:0730-2312
Publisher:Wiley (U.S.A.)
Volume:86
Number:3
Page Range:422-431
Date:20 June 2002
Official Publication:https://doi.org/10.1002/jcb.10200
PubMed:View item in PubMed

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