Alterations in cardiac dihydropyridine receptors and calcium channel function in MDX mice

Paper


Xiao, Xiao-Hui, Woolf, Peter, Watson, Michael, Lu, Sai and Hoey, Andrew. 2004. "Alterations in cardiac dihydropyridine receptors and calcium channel function in MDX mice." Walsh, R. (ed.) ISHR 2004: 18th World Congress of the International Society for Heart Research. Brisbane, Australia 07 - 11 Aug 2004 United Kingdom. https://doi.org/10.1016/j.yjmcc.2004.05.003
Paper/Presentation Title

Alterations in cardiac dihydropyridine receptors and calcium channel function in MDX mice

Presentation TypePaper
AuthorsXiao, Xiao-Hui (Author), Woolf, Peter (Author), Watson, Michael (Author), Lu, Sai (Author) and Hoey, Andrew (Author)
EditorsWalsh, R.
Journal or Proceedings TitleJournal of Molecular and Cellular Cardiology
Journal Citation37 (1), pp. 176-176
Number of Pages1
Year2004
Place of PublicationUnited Kingdom
ISSN0022-2828
1095-8584
Digital Object Identifier (DOI)https://doi.org/10.1016/j.yjmcc.2004.05.003
Web Address (URL) of Paperhttps://www.sciencedirect.com/science/article/pii/S0022282804001439
Conference/EventISHR 2004: 18th World Congress of the International Society for Heart Research
Event Details
ISHR 2004: 18th World Congress of the International Society for Heart Research
Event Date
07 to end of 11 Aug 2004
Event Location
Brisbane, Australia
Abstract

Duchenne muscular dystrophy (DMD) is a fatal neuromuscular condition affecting approximately one in 3500 live male births resulting from the lack of the myocyte protein dystrophin. The absence of dystrophin in cardiac myocytes is associated with calcium overload which in turn activates calcium-dependent proteolytic enzymes contributing to congestive heart failure, muscle necrosis and fibrosis. To date, the basis for the calcium overload has not been determined. Since L-type calcium channels are a major mediator of calcium influx we determined their potential contribution to the calcium overload. Male muscular dystrophy (mdx) mice and control C57BL10ScSn (C57) mice aged 12– 16 weeks were used in all experiments. In tissue bath studies, isolated contracting left atria from mdx revealed a reduced potency to the dihydropyridine (DHP) agonist BayK8644 and antagonist nifedipine (P < 0.05). Similarly, radioligand binding studies using the DHP antagonist [3H]-PN 200-110 showed a reduced potency (P < 0.05) in isolated membranes, associated with an increased receptor density (P < 0.05). The increased receptor density was supported by RT-PCR experiments revealing increased RNAfor the DHP receptor. Patch clamp studies revealed the presence of a diltiazem sensitive calcium current that showed delayed inactivation in isolated mdx myocytes (P < 0.01). In conclusion, the increased number of DHP binding sites and the delay in L-type current inactivation may both contribute to increased calcium influx and hence calcium overload in the dystrophin deficient mdx cardiac myocytes.

Keywordscardiac; cardiovascular systems; cell biology; mice
ANZSRC Field of Research 2020320905. Neurology and neuromuscular diseases
310106. Enzymes
320101. Cardiology (incl. cardiovascular diseases)
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Byline AffiliationsCentre for Biomedical Research
Department of Biological and Physical Sciences
Institution of OriginUniversity of Southern Queensland
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