Title of article :
Effects of different sources of copper on Ctr1, ATP7A, ATP7B, MT and DMT1 protein and gene expression in Caco-2 cells
Author/Authors :
Gao، نويسنده , , Chen and Zhu، نويسنده , , Lianqin and Zhu، نويسنده , , Fenghua and Sun، نويسنده , , Jinquan and Zhu، نويسنده , , Zuxian، نويسنده ,
Issue Information :
فصلنامه با شماره پیاپی سال 2014
Pages :
7
From page :
344
To page :
350
Abstract :
Copper sulfate (CuSO4), micron copper oxide (micron CuO) and nano copper oxide (nano CuO) at different concentrations were, respectively, added to culture media containing Caco-2 cells and their effects on Ctr1, ATP7A/7B, MT and DMT1 gene expression and protein expression were investigated and compared. The results showed that nano CuO promoted mRNA expression of Ctr1 in Caco-2 cells, and the difference was significant compared with micron CuO and CuSO4. Nano CuO was more effective in promoting the expression of Ctr1 protein than CuSO4 and micron CuO at the same concentration. Nano CuO at a concentration of 62.5 μM increased the mRNA expression levels of ATP7A and ATP7B, and the difference was significant compared with CuSO4. The addition of CuSO4 and nano CuO to the culture media promoted the expression of ATP7B proteins. CuSO4 at a concentration of 125 μM increased the mRNA expression level of MT in Caco-2 cells, and the difference was significant compared with nano CuO and micron CuO. Nano CuO at a concentration of 62.5 μM inhibited the mRNA expression of DMT1, and the difference was significant compared with CuSO4 and micron CuO. Thus, the effects of CuSO4, micron CuO and nano CuO on the expression of copper transport proteins and the genes encoding these proteins differed considerably. Nano CuO has a different uptake and transport mechanism in Caco-2 cells to those of CuSO4 and micron CuO.
Keywords :
ATP7B , ATP7A , Caco-2 cells , Ctr1 , Nano copper oxide
Journal title :
Journal of Trace Elements in Medicine and Biology
Serial Year :
2014
Journal title :
Journal of Trace Elements in Medicine and Biology
Record number :
1726014
Link To Document :
بازگشت