http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Aorta protein networks in marginal and acute zinc deficiency
Beattie, John H.,Gordon, Margaret-Jane,Rucklidge, Garry J.,Reid, Martin D.,Duncan, Gary J.,Horgan, Graham W.,Cho, Young-Eun,Kwun, In-Sook WILEY-VCH Verlag 2008 Proteomics Vol.8 No.10
<P>Human zinc deficiency is a global problem and may influence the development of cardiovascular disease. Our objective was to determine Zn deficiency affected pathways and protein interactions in rat aorta and their likely influence on stress-induced atherogenesis. In two separate studies, rats were given diets acutely (<1 mg Zn/kg) or marginally (6 mg Zn/kg) deficient in Zn. Both studies included Zn adequate controls (35 mg Zn/kg) and the acute deficiency study included a pair-fed group. After 6 wk, proteins from thoracic aorta were separated by 2-DE. Proteins affected by zinc deficiency were identified by principal component analysis. Multiple correlations of identified proteins indicated protein networks of related function. Proteins clusters decreased in zinc deficiency were related to fatty acid and carbohydrate metabolism. Structurally related proteins, including zyxin and over nine transgelin 1 proteins, were either increased or decreased by acute and marginal deficiencies. PKCα was significantly decreased in Zn deficiency suggesting that Zn may regulate the phosphorylation of target proteins. Zn deficiency-related changes in structural, carbohydrate and fatty acid-related proteins may be disadvantageous for maintaining vascular health and are consistent with a protective role for zinc in the development of atherosclerosis.</P>
Plasma zinc's alter ego is a low-molecular-weight humoral factor
Ou, Ou,Allen-Redpath, Keith,Urgast, Dagmar,Gordon, Margaret-Jane,Campbell, Gill,Feldmann, Jö,rg,Nixon, Graeme F.,Mayer, Claus-Dieter,Kwun, In-Sook,Beattie, John H. The Federation of American Societies for Experimen 2013 The FASEB Journal Vol.27 No.9
<P>Mild dietary zinc deprivation in humans and rodents has little effect on blood plasma zinc levels, and yet cellular consequences of zinc depletion can be detected in vascular and other tissues. We proposed that a zinc-regulated humoral factor might mediate the effects of zinc deprivation. Using a novel approach, primary rat vascular smooth muscle cells (VSMCs) were treated with plasma from zinc-deficient (<1 mg Zn/kg) or zinc-adequate (35 mg Zn/kg, pair-fed) adult male rats, and zinc levels were manipulated to distinguish direct and indirect effects of plasma zinc. Gene expression changes were analyzed by microarray and qPCR, and incubation of VSMCs with blood plasma from zinc-deficient rats strongly changed the expression of >2500 genes, compared to incubation of cells with zinc-adequate rat plasma. We demonstrated that this effect was caused by a low-molecular-weight (∼2-kDa) zinc-regulated humoral factor but that changes in gene expression were mostly reversed by adding zinc back to zinc-deficient plasma. Strongly regulated genes were overrepresented in pathways associated with immune function and development. We conclude that zinc deficiency induces the production of a low-molecular-weight humoral factor whose influence on VSMC gene expression is blocked by plasma zinc. This factor is therefore under dual control by zinc.—Ou, O., Allen-Redpath, K., Urgast, D., Gordon, M.-J., Campbell, G., Feldmann, J., Nixon, G. F., Mayer, C.-D., Kwun, I.-S., and Beattie, J. H. Plasma zinc's alter ego is a low-molecular-weight humoral factor.</P>