PTEN inhibits replicative senescence‐induced MMP‐1 expression by regulating NOX4‐mediated ROS in human dermal fibroblasts
Copyright policy )PTEN inhibits replicative senescence‐induced MMP‐1 expression by regulating NOX4‐mediated ROS in human dermal fibroblasts
AbstractThe biological function of NADPH oxidase (NOX) is the generation of reactive oxygen species (ROS). ROS, primarily arising from oxidative cell metabolism, play a major role in both chronological ageing and photoageing. ROS in extrinsic and intrinsic skin ageing may be assumed to induce the expression of matrix metalloproteinases. NADPH oxidase is closely linked with phosphatidylinositol 3‐OH kinase (PI3K) signalling. Protein kinase C (PKC), a downstream molecule of PI3K, is essential for superoxide generation by NADPH oxidase. However, the effect of PTEN and NOX4 in replicative‐aged MMPs expression has not been determined. In this study, we confirmed that inhibition of the PI3K signalling pathway by PTEN gene transfer abolished the NOX‐4 and MMP‐1 expression. Also, NOX‐4 down‐expression of replicative‐aged skin cells abolished the MMP‐1 expression and ROS generation. These results suggest that increase of MMP‐1 expression by replicative‐induced ROS is related to the change in the PTEN and NOX expression.
- Jeonbuk National University Korea (Republic of)
- Wonkwang University Korea (Republic of)
Short Communication, Genetic Vectors, PTEN Phosphohydrolase, Dermis, Fibroblasts, Transfection, Adenoviridae, Phosphatidylinositol 3-Kinases, Gene Expression Regulation, NADPH Oxidase 4, Humans, Matrix Metalloproteinase 1, RNA, Small Interfering, Reactive Oxygen Species, Cells, Cultured, Cellular Senescence, Protein Kinase C, Signal Transduction
Short Communication, Genetic Vectors, PTEN Phosphohydrolase, Dermis, Fibroblasts, Transfection, Adenoviridae, Phosphatidylinositol 3-Kinases, Gene Expression Regulation, NADPH Oxidase 4, Humans, Matrix Metalloproteinase 1, RNA, Small Interfering, Reactive Oxygen Species, Cells, Cultured, Cellular Senescence, Protein Kinase C, Signal Transduction
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