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Z.S. Boyd, A. Kriatchko, J. Yang, N. Agarwal, M.B. Wax, R.V. Patil; IL-10 Promotes Survival of Retinal Ganglion Cells without Activating Akt and STAT Signaling Pathways . Invest. Ophthalmol. Vis. Sci. 2003;44(13):125.
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Purpose: To examine the neuroprotective effects of the potent anti-inflammatory cytokine interleukin-10 (IL-10) following serum deprivation and dexamethasone induced apoptosis of retinal ganglion cells. Methods: Apoptosis in the rat retinal ganglion cell line (RGC-5) was induced by either serum deprivation or by dexamethasone (25 µg/ml) treatment. The anti-apoptotic effect of IL-10 was studied by assaying the cellular viability using the formazan assay as well as by YO-PRO-1 nuclear staining in flow cytometry. Activation of phosphatidylinositol (PI) 3’-kinase and STAT-3 by IL-10 was assessed by Western blotting using antibodies against phosphorylated PI3-K and STAT-3. Results: Serum deprivation and dexamethasone induced the apoptotic death in retinal ganglion cells. The viability of serum deprived retinal ganglion cells treated with IL-10 was 35% ± 3 (n = 4) after 96 h, whereas, only 16% ± 4 (n = 4) cells were viable without IL-10 treatment. These results were further confirmed by flow cytometry using YO-PRO-1 staining and determining the viability of serum deprived retinal ganglion cells with and without IL-10 treatment for 96 h. The anti-apoptotic effect of IL-10 was time- and dose-dependent and maximum effect was observed at 100 ng/ml concentration and 120 h after treatment. IL-10 treatment to the retinal ganglion cells did not increase the phosphorylation of both PI 3’-kinase and STAT-3 proteins determined by immunoblotting. Conclusions: IL-10 inhibited the serum deprived and dexamethasone induced apoptosis of retinal ganglion cells. In addition, these results demonstrated that anti-apoptotic effect of IL-10 was not by the activation of PI 3’-kinase and STAT-3 signaling pathways. It’s possible that IL-10 may exert it’s effect by modulating either nuclear factor kappaB activity or by inhibiting the synthesis of pro-inflammatory cytokines such as TNF-alpha, both of which play an important role in cell survival.
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