TY - JOUR
T1 - Altered expression of atrial natriuretic peptide and contractile protein genes in hypertrophied ventricle of JVS mice with systemic carnitine deficiency
AU - Yoshimine, Kosei
AU - Horiuchi, Masahisa
AU - Suzuki, Syusaku
AU - Kobayashi, Keiko
AU - Abdul, Jalil Md
AU - Masuda, Mina
AU - Tomomura, Mineko
AU - Ogawa, Yoshihiro
AU - Itoh, Hiroshi
AU - Nakao, Kazuwa
AU - Osame, Mituhiro
AU - Saheki, Takeyori
N1 - Funding Information:
We thank Dr M. Ohkubo for the gift of GAPDH cDNA, Ms M. Tanaka for secretarial assistance, Mr H. Tsuruta for synthesis of oligonucleotides used in this report, Mr M. Gore for editorial assistance and Mr N. Asaka for helpful advice. Supported by Grants-in-aid from the Ministry of Education, Science, and Culture of Japan, ONO Medical Research Foundation, KIMURA MEMORIAL HEART FOUNDATION and the Kodama Memorial Fund for Medical Research.
PY - 1997/2
Y1 - 1997/2
N2 - 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.
AB - 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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U2 - 10.1006/jmcc.1996.0300
DO - 10.1006/jmcc.1996.0300
M3 - Article
C2 - 9140816
AN - SCOPUS:0031079755
SN - 0022-2828
VL - 29
SP - 571
EP - 578
JO - Journal of Molecular and Cellular Cardiology
JF - Journal of Molecular and Cellular Cardiology
IS - 2
ER -