Alterations in cardiac dihydropyridine receptors and calcium channel function in MDX mice
Paper
Paper/Presentation Title | Alterations in cardiac dihydropyridine receptors and calcium channel function in MDX mice |
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Presentation Type | Paper |
Authors | Xiao, Xiao-Hui (Author), Woolf, Peter (Author), Watson, Michael (Author), Lu, Sai (Author) and Hoey, Andrew (Author) |
Editors | Walsh, R. |
Journal or Proceedings Title | Journal of Molecular and Cellular Cardiology |
Journal Citation | 37 (1), pp. 176-176 |
Number of Pages | 1 |
Year | 2004 |
Place of Publication | United Kingdom |
ISSN | 0022-2828 |
1095-8584 | |
Digital Object Identifier (DOI) | https://doi.org/10.1016/j.yjmcc.2004.05.003 |
Web Address (URL) of Paper | https://www.sciencedirect.com/science/article/pii/S0022282804001439 |
Conference/Event | ISHR 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. |
Keywords | cardiac; cardiovascular systems; cell biology; mice |
ANZSRC Field of Research 2020 | 320905. Neurology and neuromuscular diseases |
310106. Enzymes | |
320101. Cardiology (incl. cardiovascular diseases) | |
Public Notes | Files associated with this item cannot be displayed due to copyright restrictions. |
Byline Affiliations | Centre for Biomedical Research |
Department of Biological and Physical Sciences | |
Institution of Origin | University of Southern Queensland |
https://research.usq.edu.au/item/q04y0/alterations-in-cardiac-dihydropyridine-receptors-and-calcium-channel-function-in-mdx-mice
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