Effects of Selenoprotein M and Selenium on the Mitogen-Activated Protein Kinase Pathway in the Kidney of Transgenic Rat Overexpressing the Human Selenoprotein M
Effects of Selenoprotein M and Selenium on the Mitogen-Activated Protein Kinase Pathway in the Kidney of Transgenic Rat Overexpressing the Human Selenoprotein M
Ji Soon Sin(National Institute of Toxicological Research); Su Youn Yim(National Institute of Toxicological Research); Yeon Kyung Lee(Pusan National University); Chul Kyu Kim(National Institute of Toxicological Research); Byung Guk Kim(National Institute of Toxicological Research); Sun Bo Shim(National Institute of Toxicological Research); Seung Wan Jee(National Institute of Toxicological Research,); Su Hae Lee(National Institute of Toxicological Research); 배창준(국립독성연구원); Jong-Min Woo(National Institute of Toxicological Research); Sang Seop Kim(National Institute of Toxicological Research); Mi Kyong Jang(National Institute of Toxicological Research); 조정식(호서대학교); 김성만(부산대학교); Chung Yeol Lee1(Pusan National University); Kab Ryong Chae(National Institute of Toxicological Research); Dae Youn Hwang(National Institute of Toxicological Research)
24권 3호, 303~310쪽
초록
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.
Abstract
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.
- 발행기관:
- 한국실험동물학회
- 분류:
- 수의학