Altered Expression of Atrial Natriuretic Peptide and Contractile Protein Genes in Hypertrophied Ventricle of JVS Mice with Systemic Carnitine Deficiency

Yoshimine, Kosei; Horiuchi, Masahisa; Suzuki, Syusaku; Kobayashi, Keiko; Abdul, Jalil Md.; Masuda, Mina; Tomomura, Mineko; Ogawa, Yoshihiro; Itoh, Hiroshi; Nakao, Kazuwa; Osame, M; Saheki, Takeyori

doi:10.1006/jmcc.1996.0300

Cited by 20 publications

(12 citation statements)

References 3 publications

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“…One of the features of dilated cardiomyopathy is the upregulation of cardiac hormones such as natriuretic peptides as a compensatory mechanism to maintain cardiac output (17,18). Upregulation of genes involved in sarcomere organization also occurs (19,20).…”

Section: Resultsmentioning

confidence: 99%

Mitogen-Activated Protein Kinase Inhibitors Improve Heart Function and Prevent Fibrosis in Cardiomyopathy Caused by Mutation in Lamin A/C Gene

et al. 2011

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Background-Mutations in the lamin A/C gene, LMNA, can cause dilated cardiomyopathy. We have shown abnormal activation of the extracellular signal-regulated kinase (ERK) and the c-jun N-terminal kinase (JNK) branches of the mitogen-activated protein kinase signaling cascade in hearts from Lmna H222P/H222P mice that develop dilated cardiomyopathy. We recently showed that partial inhibition of ERK and JNK signaling before the onset of cardiomyopathy in Lmna H222P/H222P mice prevented the development of left ventricle dilatation and decreased cardiac ejection fraction at a time when they occurred in untreated mice. Methods and Results-To determine whether pharmacological inhibitors of ERK and JNK signaling could be clinically useful to treat cardiomyopathy caused by LMNA mutation, we administered them to Lmna H222P/H222P mice after they developed left ventricular dilatation and decreased ejection fraction. Lmna H222P/H222P mice were treated with ERK and JNK signaling inhibitors from 16 to 20 or, in pilot experiments, 19 to 24 weeks of age. The inhibitors blocked increased expression of RNAs encoding natriuretic peptide precursors and proteins involved in sarcomere architecture that occurred in placebo-treated mice. Echocardiography and histological analysis demonstrated that treatment prevented left ventricular end-systolic dilatation, increased ejection fraction, and decreased myocardial fibrosis. Conclusion-Inhibitors

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Section: Resultsmentioning

confidence: 99%

Mitogen-Activated Protein Kinase Inhibitors Improve Heart Function and Prevent Fibrosis in Cardiomyopathy Caused by Mutation in Lamin A/C Gene

et al. 2011

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“…25,40,50,56 Current data and other reports therefore support the idea that deflazacort-induced hypertrophy and increased ␣-cardiac MHC occurred largely independent of the renin-angiotensin system. 21,27,35,57 Protection from contraction-induced damage may derive from combined increases in laminin, tau- rine, and bFGF that could stabilize membranes, mediate calcium homeostasis, and protect against peroxidation injury, respectively. 1,14,15,23,45 The correlative pattern of cellular and metabolic changes here suggests that H-NMRS was able to track evolving cardiomyopathy and treatment effects.…”

Section: Discussionmentioning

confidence: 99%

“…The ratio of ␣-to ␤-cardiac myosin isoforms can provide an index of oxidative and glycolytic capacity, respectively. 18,19,25,50,57 The ␣-cardiac myosin heavy chain (MHC) distribution and concentration may also change during disease and treatment with glucocorticoids. 12 Proton magnetic resonance spectroscopy (H-NMRS) can detect metabolic changes of disease and treatment.…”

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confidence: 99%

Metabolic shifts and myocyte hypertrophy in deflazacort treatment ofmdx mouse cardiomyopathy

Skrabek

Anderson

2001

Muscle Nerve

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“…Increases in ventricular expression of ANF have been documented in experimental models of heart failure and cardiomyopathy (29,38,(52)(53)(54)(55) as well as in human heart failure (56). Our analysis identified 104 and 114 genes that were differentially expressed in hearts from Lmna H222P/+ and Lmna H222P/H222P mice, respectively.…”

Section: Figurementioning

confidence: 99%

Activation of MAPK pathways links LMNA mutations to cardiomyopathy in Emery-Dreifuss muscular dystrophy

Muchir¹,

Pavlidis²,

Decostre³

et al. 2007

J. Clin. Invest.

269

339

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Altered Expression of Atrial Natriuretic Peptide and Contractile Protein Genes in Hypertrophied Ventricle of JVS Mice with Systemic Carnitine Deficiency

Cited by 20 publications

References 3 publications

Mitogen-Activated Protein Kinase Inhibitors Improve Heart Function and Prevent Fibrosis in Cardiomyopathy Caused by Mutation in Lamin A/C Gene

Mitogen-Activated Protein Kinase Inhibitors Improve Heart Function and Prevent Fibrosis in Cardiomyopathy Caused by Mutation in Lamin A/C Gene

Metabolic shifts and myocyte hypertrophy in deflazacort treatment ofmdx mouse cardiomyopathy

Activation of MAPK pathways links LMNA mutations to cardiomyopathy in Emery-Dreifuss muscular dystrophy

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