Skip to main content
ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Healthy Body Weight Research » Research » Publications at this Location » Publication #179965
Title: COPPER DEFICIENCY INCREASES FIBULIN-5 (DANCE/EVEC) BUT DECREASES CYTOCHROME C OXIDASE VIB EXPRESSION IN RAT HEART

Author
item Zeng, Huawei
item Saari, Jack
item Dahlen, Gwen

Submitted to: Inorganic Biochemistry
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/2/2005
Publication Date: 12/20/2005
Citation: Zeng, H., Saari, J.T., Dahlen, G.M. 2005. Copper deficiency increases fibulin-5 (dance/evec) but decreases cytochrome c oxidase vib expression in rat heart. Inorganic Biochemistry. 100:186-91.

Interpretive Summary: Copper is an essential trace element for humans. It has been well documented that dietary copper (Cu) deficiency causes a hypertrophic cardiomyopathy in rodent models. However, a possible alteration in gene expression has not been fully examined. The present study was undertaken to determine the effect of Cu deficiency on protein profiles in rat heart tissue with the combination of the isotope-coded affinity tag (ICAT) method and Western blotting analysis. Our data demonstrated that there was an 85% increase in developmental arteries and neural crest EGF-like (DANCE) protein and a 2.4 fold decrease in cytochrome C oxidase VIb subunit, but no change in succinate-ubiquinol oxidoreductase IP subunit in Cu-deficient rat heart. Collectively, these results may explain the molecular basis for the observed balloon-injured arteries and mitochondrial impairment in Cu-deficient rats that exhibit hypertrophic-cardiomyopathy. These findings will be useful information for scientists and health-care professionals who are interested in copper nutrition and heart disease.

Technical Abstract: It has been well documented that dietary copper (Cu) deficiency causes a hypertrophic cardiomyopathy in rodent models. However, a possible alteration in gene expression has not been fully examined. The present study was undertaken to determine the effect of Cu deficiency on protein profiles in rat heart tissue with the combination of the isotope-coded affinity tag (ICAT) method and Western blotting analysis. Male Sprague-Dawley rats were fed diets that were either Cu-adequate (6.0 µg Cu/g diet n = 6) or Cu-deficient (0.3 µg Cu/g diet n = 6) for 5 wk. The high-salt buffer (HSB) protein profiles from heart tissue of Cu-deficient rats were different from those of Cu-adequate rats; and there were seven major protein species differed by more than 2 fold. With three available antibodies, our Western blotting analysis confirmed that there was an 85% increase in developmental arteries and neural crest EGF-like (DANCE) protein and a 2.4 fold decrease in cytochrome C oxidase VIb subunit, but no change in succinate-ubiquinol oxidoreductase IP subunit in Cu-deficient rat heart. Collectively, these results may explain the molecular basis for the observed balloon-injured arteries and mitochondrial impairment in Cu-deficient rat that exhibit hypertrophic-cardiomyopathy.