Effect of microRNA-210 induced by deferoxamine on iron metabolism in rat L6 skeletal cell

• Main Authors: Han-Chich Feng, 酆涵之
• Other Authors: Yih-Fong Liew
• Format: Others
• Language: zh-TW
• Published: 2014
• Online Access: http://ndltd.ncl.edu.tw/handle/93466718273463263671

碩士 === 輔仁大學 === 營養科學系碩士班 === 102 === MicroRNA-210 (miR-210) is a small non-coding RNA, which over-expressing modulates iron metabolism, proliferation and apoptosis. Our previous study has demonstrated both dietary iron deficiency and iron chelator increase miR-210 level in skeletal muscle; however, the physiological and biochemical function by iron deficiency in skeletal muscle is still unrevealed. Therefore, the aim of present study is to establish the miR-210 expression which is lower to the normal rat’s muscle cells model by transfect antisense miRNA-210 vector to investigate the effect of microRNA-210 induced by DFO treatment on iron metabolism in rat L6 skeletal cell. The expression of miR-210 levels was decreased about 50% by transfection of antisense miR-210 vector in L6 skeletal muscle cell. The mitochondrial IscU protein levels, cytosolic aconitase activity and H-ferritin protein levels are increased in anti-miR-210 treated L6 cell. Moreover, the mitochondrial reactive oxygen species (ROS) also increase in anti-miR-210 cell. The mitochondrial aconitase activity, cytosolic aconitase activity, which protein levels were significantly decreased by DFO treatment, whereas the mitochondrial aconitase protein levels remained unchanged. Furthermore, miR-210 expression is delay increased, at the same time reduced IscU and H-ferritin protein levels, but no effect in mitochondrial ROS production in anti-miR-210 cell by DFO treatment. In summary, the expression of miR-210 expression under normal physiological condition suggests it might be involved in regulation of iron metabolism and balance intracellular redox status. However, the up-regulation of miR-210 expression by iron deficiency may protect the cell.