Matz J M, Blake M J, Saari J T, Bode A M
Department of Physiology, University of North Dakota School of Medicine, Grand Forks 58202.
FASEB J. 1994 Jan;8(1):97-102.
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.
膳食铜缺乏通过抑制儿茶酚胺代谢以及改变心脏线粒体的结构和功能来损害心血管功能。热休克蛋白（HSPs）是一组细胞内稳态蛋白，在暴露于应激后，通过儿茶酚胺能传递在血管组织中被诱导产生。我们研究了膳食铜缺乏对几种心血管组织中热休克蛋白的诱导和积累的影响。与铜充足（CuA）的对照组相比，铜缺乏（CuD）大鼠中应激诱导的主动脉HSP70 mRNA水平降低。可卡因诱导的HSP70 mRNA积累在CuA和CuD大鼠之间没有差异，这表明在受限制的CuD动物中HSP70水平降低可能是由于儿茶酚胺能神经传递改变所致。CuD大鼠心房中HSP60 mRNA水平特异性降低，这可能与线粒体结构和功能改变有关。这些结果描述了膳食铜缺乏与高度保守的细胞应激反应蛋白表达之间的一种新关系。血管组织中这些必需的内稳态蛋白的缺失可能导致已知伴随铜缺乏的心血管功能损害。
