Altered expression of atrial natriuretic peptide and contractile protein genes in hypertrophied ventricle of JVS mice with systemic carnitine deficiency

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

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

To characterize cardiac hypertrophy in juvenile visceral steatosis (JVS) mice with systemic carnitine deficiency, we investigated how the hypertrophy develops and whether it is associated with altered expression of any specific genes, especially atrial natriuretic peptide (ANP) and contractile protein genes, in the hypertrophied ventricle. Cardiac hypertrophy in JVS mice became apparent at 10 days after birth and progressed during development. The hypertrophy was observed in the ventricles but not in the atria. ANP mRNA was more intensively expressed in JVS ventricles than in control even at 5 days. Carnitine administration ameliorated the cardiac hypertrophy and suppressed the augmentation of ANP mRNA in the ventricles. Isoform change of expression of α-actin genes from cardiac to skeletal was seen in the ventricles of JVS mice at 2 weeks. There was no difference in the ratio of β-myosin heavy chain mRNA to α-myosin heavy chain mRNA between control and JVS mice at 5 days, but at 2 weeks the ratio was significantly lower in JVS mice than in control. These results suggest that the molecular characteristics of cardiac hypertrophy caused by carnitine deficiency are different from those of cardiac hypertrophy caused by aortic constriction.

Original languageEnglish
Pages (from-to)571-578
Number of pages8
JournalJournal of Molecular and Cellular Cardiology
Volume29
Issue number2
DOIs
Publication statusPublished - 1997 Feb
Externally publishedYes

Fingerprint

Contractile Proteins
Atrial Natriuretic Factor
Fatty Liver
Cardiomegaly
Genes
Messenger RNA
Myosin Heavy Chains
Carnitine
Hypertrophy
Constriction
Systemic carnitine deficiency
Actins
Protein Isoforms
Parturition
Gene Expression

Keywords

  • α-actin
  • Animal model
  • Atrial natriuretic peptide
  • Cardiac hypertrophy
  • Carnitine deficiency
  • JVS mice
  • Myosin heavy chain

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine

Cite this

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, Mituhiro; Saheki, Takeyori.

In: Journal of Molecular and Cellular Cardiology, Vol. 29, No. 2, 02.1997, p. 571-578.

Research output: Contribution to journalArticle

Yoshimine, K, Horiuchi, M, Suzuki, S, Kobayashi, K, Abdul, JM, Masuda, M, Tomomura, M, Ogawa, Y, Itoh, H, Nakao, K, Osame, M & Saheki, T 1997, 'Altered expression of atrial natriuretic peptide and contractile protein genes in hypertrophied ventricle of JVS mice with systemic carnitine deficiency', Journal of Molecular and Cellular Cardiology, vol. 29, no. 2, pp. 571-578. https://doi.org/10.1006/jmcc.1996.0300
Yoshimine, Kosei ; Horiuchi, Masahisa ; Suzuki, Syusaku ; Kobayashi, Keiko ; Abdul, Jalil Md ; Masuda, Mina ; Tomomura, Mineko ; Ogawa, Yoshihiro ; Itoh, Hiroshi ; Nakao, Kazuwa ; Osame, Mituhiro ; Saheki, Takeyori. / Altered expression of atrial natriuretic peptide and contractile protein genes in hypertrophied ventricle of JVS mice with systemic carnitine deficiency. In: Journal of Molecular and Cellular Cardiology. 1997 ; Vol. 29, No. 2. pp. 571-578.
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abstract = "To characterize cardiac hypertrophy in juvenile visceral steatosis (JVS) mice with systemic carnitine deficiency, we investigated how the hypertrophy develops and whether it is associated with altered expression of any specific genes, especially atrial natriuretic peptide (ANP) and contractile protein genes, in the hypertrophied ventricle. Cardiac hypertrophy in JVS mice became apparent at 10 days after birth and progressed during development. The hypertrophy was observed in the ventricles but not in the atria. ANP mRNA was more intensively expressed in JVS ventricles than in control even at 5 days. Carnitine administration ameliorated the cardiac hypertrophy and suppressed the augmentation of ANP mRNA in the ventricles. Isoform change of expression of α-actin genes from cardiac to skeletal was seen in the ventricles of JVS mice at 2 weeks. There was no difference in the ratio of β-myosin heavy chain mRNA to α-myosin heavy chain mRNA between control and JVS mice at 5 days, but at 2 weeks the ratio was significantly lower in JVS mice than in control. These results suggest that the molecular characteristics of cardiac hypertrophy caused by carnitine deficiency are different from those of cardiac hypertrophy caused by aortic constriction.",
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