Effects of Selenoprotein M and Selenium on the Mitogen-Activated Protein Kinase Pathway in the Kidney of Transgenic Rat Overexpressing the Human Selenoprotein M

Selenium and selenoprotein are tightly associated with the protective and antioxidant effects against damage induced by various metal ions in the kidney. Many effects of these kidney damage and stress are mediated by the mitogen-activated protein kinase signaling pathways. To investigate whether selenium treatment and selenoprotein M overexpression would impact on the mitogen-activated protein kinase pathway in the kidney, we detected the phosphorylation level of major components involving p38 kinase, c-jun N-terminal kinase and extracellular signaling-regulated kinase in the transgenic rat overexpressing human selenoprotein M gene. At first, western blot analysis showed that transgenic rats used in this study had the highly expression level of selenoprotein M in the kidney tissue, respectively. The phosphorylation level of p38 kinase was slightly increased in the wild-type rats of selenium-treated group, while did not change in the transgenic rats. Also, the phosphorylation level of c-jun N-terminal kinase was very similar with the change patterns of p38 kinase. Especially, extracellular signaling-regulated kinase was significantly inhibited in the selenium-treatment group. Furthermore, this inhibition rate of extracellular signaling-regulated kinase was stimulated by selenium M overexpression in the transgenic rats. These results suggest that the overexpression of selenoprotein M could effectively influenced the kidney cell proliferation, differentiation and apoptosis through the inhibition of extracellular signaling-regulated kinase in the kidney tissue of transgenic rat.