Post-infarction left ventricular remodeling induces changes in creatine kinase mRNA and protein subunit levels in porcine myocardium

Chuong D. Hoang, Jianyi Zhang, R. Payne, Fred S. Apple

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Energy metabolism is altered in post-infarction remodeled pig myocardium. To understand the basis of this abnormality, we examined the pattern of creatine kinase (CK) gene expression and the relative content of CK protein subunits in pig hearts with proximal left circumflex coronary artery ligation. At 2 months after infarct, both Northern and Western blot analyses were performed on left ventricular myocardium remote from the infarct zone in ligation animals (n = 8). Results were compared with data from the left ventricular myocardium from similar sized normal (control pigs (n = 7). Steady-state levels of mitochondrial CK mRNA decreased 46% in left ventricular remodeled (LVR) heart samples (93.40 ± 18.60 arbitrary units) compared with controls (172.85 ± 37.20 arbitrary units), whereas CK-M subunit mRNA levels remained unchanged between the control and LVR groups (319.50 ± 35.25 and 352.50 ± 62.18 arbitrary units, respectively). The mean control group CK-M protein subunits (2.04 ± 0.31 arbitrary units) decreased 53% (P <0.05) compared with the LVR group (0.95 ± 0.25 arbitrary units). Similarly, the mean control group (n = 4) mitochondrial CK protein subunits (1.12 ± 0.04 arbitrary units) decreased 30% (P <0.05) compared with the LVR group (n = 4; 0.79 ± 0.06 arbitrary units). Mean CK-B protein subunits in LVR pig hearts (0.84 ± 0.23 arbitrary units) increased 77% compared with control (0.48 ± 0.05 arbitrary units). The total CK activity did not change significantly between control hearts at 164 ± 11 IU/mg and LVR at 212 ± 32 IU/mg. We suggest that these alterations of the CK system represent the bioenergetic phenotype of LVR myocardium at the molecular level. The CK system response may ultimately prove inadequate in meeting the abnormal energy requirements of remodeled heart and, therefore, may contribute to the transition toward failure.

Original languageEnglish (US)
Pages (from-to)257-264
Number of pages8
JournalAmerican Journal of Pathology
Volume151
Issue number1
StatePublished - 1997
Externally publishedYes

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Ventricular Remodeling
Protein Subunits
Creatine Kinase
Infarction
Myocardium
Swine
Messenger RNA
Mitochondrial Form Creatine Kinase
MM Form Creatine Kinase
Energy Metabolism
Ligation
Control Groups
Northern Blotting
Coronary Vessels
Western Blotting
Phenotype
Gene Expression

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

Post-infarction left ventricular remodeling induces changes in creatine kinase mRNA and protein subunit levels in porcine myocardium. / Hoang, Chuong D.; Zhang, Jianyi; Payne, R.; Apple, Fred S.

In: American Journal of Pathology, Vol. 151, No. 1, 1997, p. 257-264.

Research output: Contribution to journalArticle

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abstract = "Energy metabolism is altered in post-infarction remodeled pig myocardium. To understand the basis of this abnormality, we examined the pattern of creatine kinase (CK) gene expression and the relative content of CK protein subunits in pig hearts with proximal left circumflex coronary artery ligation. At 2 months after infarct, both Northern and Western blot analyses were performed on left ventricular myocardium remote from the infarct zone in ligation animals (n = 8). Results were compared with data from the left ventricular myocardium from similar sized normal (control pigs (n = 7). Steady-state levels of mitochondrial CK mRNA decreased 46{\%} in left ventricular remodeled (LVR) heart samples (93.40 ± 18.60 arbitrary units) compared with controls (172.85 ± 37.20 arbitrary units), whereas CK-M subunit mRNA levels remained unchanged between the control and LVR groups (319.50 ± 35.25 and 352.50 ± 62.18 arbitrary units, respectively). The mean control group CK-M protein subunits (2.04 ± 0.31 arbitrary units) decreased 53{\%} (P <0.05) compared with the LVR group (0.95 ± 0.25 arbitrary units). Similarly, the mean control group (n = 4) mitochondrial CK protein subunits (1.12 ± 0.04 arbitrary units) decreased 30{\%} (P <0.05) compared with the LVR group (n = 4; 0.79 ± 0.06 arbitrary units). Mean CK-B protein subunits in LVR pig hearts (0.84 ± 0.23 arbitrary units) increased 77{\%} compared with control (0.48 ± 0.05 arbitrary units). The total CK activity did not change significantly between control hearts at 164 ± 11 IU/mg and LVR at 212 ± 32 IU/mg. We suggest that these alterations of the CK system represent the bioenergetic phenotype of LVR myocardium at the molecular level. The CK system response may ultimately prove inadequate in meeting the abnormal energy requirements of remodeled heart and, therefore, may contribute to the transition toward failure.",
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