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The role of mTOR signalling in RGC axon regeneration

Wilhelm, Annika (2011)
M.Res. thesis, University of Birmingham.

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Axons from the central nervous system (CNS) do not regenerate, causing a major problem for recovery after CNS injury. One possible reason why axon growth is inhibited is intracellular suppression of growth signals. In this work, we examined the role of RTP801 during axon regeneration in vitro and in vivo. RTP801 is an upstream inhibitor of mTOR signalling, which is central to cell growth. We report here that retinal ganglion cells (RGC) in vitro and in vivo responded to siRNA designed against RTP801 (siRTP801). Due to a limited amount of time not all experiments could be repeated in triplicate however a trend shows that siRTP801 treatment does not enhance RGC survival or neurite outgrowth in vitro but increases neurite length. Treatment with siRTP801 in combination with ciliary neurotrophic factor (CNTF) and an anti-apoptotic caspase-2 inhibitor seems to be most effective in promoting long RGC neurites.
The in vitro results support the data from the in vivo work where an increase of long distant axons has been documented. However, the generated data is not conclusive and more experiments need to be carried out. Nevertheless, these findings demonstrate a potential for siRTP801 as a novel strategy to enhance axon regeneration in RGC.

Type of Work:M.Res. thesis.
Supervisor(s):Logan, Ann and Ahmed, Zubar
School/Faculty:Colleges (2008 onwards) > College of Medical & Dental Sciences
Department:School of Clinical and Experimental Medicine
Subjects:RC Internal medicine
Institution:University of Birmingham
ID Code:2947
This unpublished thesis/dissertation is copyright of the author and/or third parties. The intellectual property rights of the author or third parties in respect of this work are as defined by The Copyright Designs and Patents Act 1988 or as modified by any successor legislation. Any use made of information contained in this thesis/dissertation must be in accordance with that legislation and must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the permission of the copyright holder.
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