Regulation of Nell2 in the senescence-accelerated mouse andelucidation of axonal extension.

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The senescence-accelerated mouse (SAM) has been established as a model of accelerated aging. SAM consists of the senescence-accelerated prone mouse (SAMP) and senescence-accelerated resistant mouse (SAMR), which exhibits normal aging process. We investigated the change of retinal ganglion cell (RGC) and Sirtuin 1 (Sirt1), which is a member of the sirtuin family of proteins and related with aging process, and Nell2, which is involved in neuronal growth process, in SAMR, SAMP8, and SAMP10. RGC in3 month old SAMP8 and P10 was significantly decreased, compared with those in SAMR. No significant changes in the INL and the ONL were observed in SAMR, SAMP8, and SAMP10. IB showed that a significant decrease in Sirt1 and Nell2 were observed in the retinas of SAMP8 and SAMP10, compared to SAMR. An abundant Sirt1 was seen in the RGC and the IPLof SAMR retina, compared to those in SAMP8 and SAMP10.