Linked Life Data

21421818

Source:http://linkedlifedata.com/resource/pubmed/id/21421818

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pubmed-article:21421818pubmed:abstractTextMice with three amino acid mutations in the calmodulin binding domain of type-2 ryanodine receptor ion channel (Ryr2(ADA/ADA) mice) have impaired intracellular Ca(2+) handling and cardiac hypertrophy with death at an early age. In this report, the role of signaling molecules implicated in cardiac hypertrophy of Ryr2(ADA/ADA) mice was investigated. Calcineurin A-? (CNA-?) and nuclear factor of activated T cell (NFAT) signaling were monitored in mice carrying either luciferase transgene driven by NFAT-dependent promoter or knockout of CNA-?. NFAT transcriptional activity in Ryr2(ADA/ADA) hearts was not markedly upregulated at embryonic day 16.5 compared with wild-type but significantly increased at postnatal days 1 and 10. Ablation of CNA-? extended the life span of Ryr2(ADA/ADA) mice and enhanced cardiac function without improving sarcoplasmic reticulum Ca(2+) handling or suppressing the expression of genes implicated in cardiac hypertrophy. Embryonic day 16.5 Ryr2(ADA/ADA) mice had normal heart weights with no major changes in Akt1 and class II histone deacetylase phosphorylation and myocyte enhancer factor-2 activity. In contrast, phosphorylation levels of Erk1/2, p90 ribosomal S6 kinases (p90RSKs), and GSK-3? were increased in hearts of embryonic day 16.5 homozygous mutant mice. The results indicate that an impaired calmodulin regulation of RyR2 was neither associated with an altered CNA-?/NFAT, class II histone deacetylase (HDAC)/MEF2, nor Akt signaling in embryonic day 16.5 hearts; rather increased Erk1/2 and p90RSK phosphorylation levels likely leading to reduced GSK-3? activity were found to precede development of cardiac hypertrophy in mice expressing dysfunctional ryanodine receptor ion channel.lld:pubmed
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pubmed-article:21421818pubmed:dateRevised2011-11-2lld:pubmed
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pubmed-article:21421818pubmed:year2011lld:pubmed
pubmed-article:21421818pubmed:articleTitleDysfunctional ryanodine receptor and cardiac hypertrophy: role of signaling molecules.lld:pubmed
pubmed-article:21421818pubmed:affiliationDept. of Biochemistry and Biophysics, Univ. of North Carolina, Chapel Hill, NC 27599-7260, USA.lld:pubmed
pubmed-article:21421818pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:21421818pubmed:publicationTypeResearch Support, N.I.H., Extramurallld:pubmed
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