Abstract
Facilitative glucose transporter member 10 (GLUT10) protein, also known SLC2A10 gene, belong to the class III GLUT family. Recent studies have been reported SLC2A10 gene mutation caused arterial tortuosity syndrome (ATS). Our laboratory previously demonstrated that GLUT10 is localized to the mitochondria and mediated dehydroascorbic acid (DHA) transport into mitochondria to reduced reactive oxygen species (ROS) production. However the molecular mechanisms of GLUT10 targeting mitochondria are still obscure. We hypothesis that GLUT10 targeting to mitochondria were regulated by external-stimulus in the A10 cell. Here, we used confocal image data and Imaris software further analysis the levels of GLUT10 spot pattern percentage, which co-localized with mitochondria, were increased upon long-term H2O2 treatment but not glucose and insulin stimulation. These results indirectly revealed the functions of GLUT10 that reduced mitochondrial ROS production through increased levels of mitochondria targeting. It is concluded that GLUT10 has response to ROS and increase the mitochondria targeting percentage upon long-term H2O2 stimulation.