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제109회 대한화학회 학술발표회, 총회 및 기기전시회 안내 Mitochondrial ROS and Cell Senescence

2012년 2월 28일 08시 56분 06초
BIO1-4 이곳을 클릭하시면 발표코드에 대한 설명을 보실 수 있습니다.
목 16시 : 25분
생명화학 - Reactive oxygen species in age-related diseases
저자 및
아주대학교 의과대학 생화학교실, Korea
Functional defects of mitochondria have long been implicated in cellular aging process. However, its detailed underlying mechanism of how mitochondrial dysfunction is involved in cellular senescence remains unclear. Recently, we clearly demonstrated that respiratory defects are tightly linked with the prolonged generation of reactive oxygen species (ROS) by employing transforming growth factor β1 (TGF β1), a cytokine. TGF β1 induced senescence of Mv1Lu cell by persistently producing mitochondrial reactive oxygen species (ROS) through decreased complex IV activity. During the process glycogen synthase kinase 3 (GSK3) was progressively phosphorylated, corresponding well to the intracellular ROS generation profile. Unexpectedly, this GSK3 phosphorylation was found to be an upstream event of the ROS generation. Moreover, we found that GSK3 substantially exists in mitochondria of Mv1Lu cell and binds complex IV subunit 6b which has no electron carrier and is topologically located in the mitochondrial intermembrane space. Involvement of subunit 6b in controlling complex IV activity and overall respiration rate was proved with siRNA-mediated knockdown of subunit 6b. Finally, TGF β1 treatment decreased the binding of the subunit 6b to GSK3 and subunit 6b phosphorylation. Taken together, our results suggest that GSK3 inactivation is importantly involved in TGF β1-induced complex IV defects through decreasing phosphorylation of the subunit 6b, thereby contributing to senescence-associated mitochondrial ROS generation.