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TAK-1 inhibition accelerates cellular senescence of retinal pigment epithelial cells, possible new pathway causing early stages of AMD

Poster Details

First Author: A.Pollack ISRAEL

Co Author(s):    Z. Dvashi                  0   0 0   0 0   0 0   0 0

Abstract Details


This study aimed to investigate the role of the transforming growth factor-beta-activated kinase 1 (TAK1) in cellular senescence and apoptosis of the retinal pigment epithelium (RPE) cells, as a model for dry age-related macular degeneration (AMD). RPE cells are subjected to a high level of oxidative stress from several sources, which can contribute to the development early AMD. However, the precise mechanism is unclear. One possible pathway involves cellular senescence of the RPE cells that share similar feature to cell atrophy. Interestingly, TAK-1 was reported to be involved in the response to stress in variety of cells.


Kaplan Medical Center, Rehovot, affiliated to the Hebrew University, Jerusalem, Israel.


ARPE-19 tissue culture cells were used to study the role of TAK-1 in the hemostasis of RPE cells. cells were subjected to FACS analysis, immunofluorescence staining, XTT analysis, western blots analysis and real time PCR. Cells were treated with oxidative stress with or without TAK-1 inhibitor (5z-7 oxozeaenol). Cells were harvested and subjected to analysis in the different methods


Inhibition of the TAK-1 kinase activity reduced the rate of apoptotic RPE cells and shifted the cells to cellular senescence upon oxidative damage. Moreover, TAK-1 inhibition altered the expression of p53, which is the hall-mark of apoptosis, thus affecting the signal-transduction which underlies this process. The aberrant signal transduction led to increase of the senescence phenotype, accompanied by: 1. augmented SA-beta-gal expression 2. pigmentary and 3.morphology abnormalities. Finally, the inhibition of TAK-1 affected RPE cells similarly to changes that characterize early AMD


This study demonstrates that TAK-1 is involved in the response of RPE cells to oxidative stress. Cells in which TAK-1 was inhibited displayed phenotypes similar to those associated with dry AMD. Furthermore, our results revealed that TAK-1 is essential to the maintenance of healthy RPE cells by regulating p53 This data may imply a potential novel approach to maintain the RPE cells, thus may halt the progression of dry AMD.

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