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W. Jahng, S. R. Sripathi, S. Marwana, Z. Liu, T. Moser, E. Hager; Prohibitin as a New Mediator of Mitochondria Shuttling. Invest. Ophthalmol. Vis. Sci. 2010;51(13):1686.
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Prohibitin is a potential tumor suppressor with anti proliferative activity. It is a regulator of cell cycle progression and plays a major role in apoptosis. Prohibitin is highly conserved from bacteria to human, but its presence and function in the eye has not yet been studied. We have found that mitochondrial prohibitin is initially down-regulated in mild oxidative stress in the RPE. We will test our hypotheses that prohibitin acts as a chaperone protein in pigmentation, mitochondria-nucleus translocation, and aging processes.
Proteomic data from an in vivo mouse model in constant light and in vitro RPE D 407 model were compared to control. The functional role of prohibitin in the retina and the RPE was studied using biochemical methods such as 2D differential gel electrophoresis, immunohistochemistry, western blot, and computational analysis. Mitochondria-nucleus shuttling is studied using the Cox method. Prohibitin expression was studied using an aging model in vivo.
Prohibitin was found to be one of the early molecules of oxidative stress in the RPE and the retina. Mitochondrial prohibitin is down-regulated in the RPE under oxidative stress. However, it is up-regulated in the retina and localized in ganglion cell outer nuclear and inner nuclear layers. Comparison of expression level changes with other apoptotic markers, and translocalization between mitochondria and the nucleus imply that the regulation of prohibitin is an early signaling event of apoptosis in the RPE and the retina under oxidative stress.
Our studies have identified prohibitin as a new mediator of mitochondria shuttling that is operative under conditions of oxidant stress.
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