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Y. Song, L. Zhao, Y. Liu, Y. Li, A.M. Laties, R. Wen; Negative Regulation of Phototransduction Machinery by CNTF Is Likely Through the Photostasis Mechanism . Invest. Ophthalmol. Vis. Sci. 2005;46(13):163.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: While CNTF protects photoreceptors against degeneration, it also diminishes ERG wave amplitude. Our previous findings indicate that the ERG suppression was due to negative regulation of the phototransduction machinery. The present work investigates effects on phototransduction machinery by CNTF and by bright light exposure. Methods: Human CNTF cDNA was PCR–cloned, expressed in E. coli. Recombinant protein was purified on Ni+ columns under native conditions. Eyes of Long Evans (LE) rats were injected intravitreally with CNTF protein (10 µg in 5 µl) or PBS (5 µl). Retinas were harvested 6 days and 3 weeks after injection. For light exposure experiments, LE rats were exposed to 400 lux light for 10 hrs (8am to 6pm) every day for 7 days. Retinas were harvested immediately after the 7–day exposure and 2 weeks later. Levels of phototransduction–related proteins were evaluated on Western blots. Photoreceptor morphology was examined in semi–thin plastic sections. Results: Six days after CNTF injection treated eyes experienced significant decrease in rhodopsin expression, along with a marked increase in arrestin protein. In addition, the length of rod outer segments was shortened by 30–50%. All changes were recovered 3 weeks after injection. Comparable changes were found in animals exposed to bright light for 7 days, including rhodopsin and arrestin expression, as well as shortened ROS length. The changes in bright light exposed animals were also recovered in 2 weeks. Conclusions: CNTF or light exposure regulates the phototransduction machinery in a similar fashion. It is believed that bright light exposure regulates the phototransduction machinery by the photostasis mechanism. Our results therefore suggest that CNTF invokes the same or a similar mechanism.
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