Dietary copper deficiency reduces heat shock protein expression in cardiovascular tissues

Jeannine M. Matz, Michael J. Blake, Jack T. Saari, Ann M. Bode

Research output: Contribution to journalArticlepeer-review

15 Scopus citations

Abstract

Dietary copper deficiency impairs cardiovascular function by depression of catecholamine metabolism, and alteration of the structure and function of cardiac mitochondria. Heat shock proteins (HSPs) are a group of cellular homeostatic proteins that are induced in vascular tissue by catecholaminergic transmission after exposure to stress. We investigated the effects of dietary copper deficiency on the induction and accumulation of HSPs in several cardiovascular tissues. Stress-induced levels of aortic HSP70 mRNA were reduced in copper-deficient (CuD) rats when compared with copper-adequate (CuA) controls. Cocaine-induced HSP70 mRNA accumulation was not different between CuA and CuD rats, suggesting that reduced HSP70 levels in restrained CuD animals may result from altered catecholaminergic neurotransmission. The level of HSP60 mRNA was specifically reduced in the atria of CuD rats, which may be associated with altered mitochondrial structure and function. These results describe a novel relationship between dietary copper deficiency and the expression of highly conserved cellular stress response proteins. Loss of these essential homeostatic proteins in vascular tissue may contribute to the impairment of cardiovascular function known to accompany copper deficiency.

Original languageEnglish (US)
Pages (from-to)97-102
Number of pages6
JournalFASEB Journal
Volume8
Issue number1
DOIs
StatePublished - 1994
Externally publishedYes

Keywords

  • cardiac mitochondria
  • catecholamine metabolism
  • metabolic stressors

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