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Huang et al. (900) analyzed the level of HSP27 phosphorylation in experimental rat and in spontaneous DBA/2J mouse glaucoma models. In both these models elevated intraocular pressure (IOP) leads to RGC death. This study utilized immunoblot and immunohistochemestry for quantitative and spatial analysis of HSP27 induction in the retinas of IOP elevated eyes. The level of total HSP27 was found to be elevated ~ 4 and 3 fold in experimental model and DBA/2J, respectively. pHSP27 was also increased in both models ~ 2 fold. Increased HSP27 and pHSP27 were immunolocalized mainly to glial cells but were also present in RGCs and NFL. Authors suggest that phosphorylation of HSP27 is a fundamental biological response to elevated IOP. However, since the levels of both HSP27 and pHSP27 are increased, it is not clear whether the phosphorylation is specifically induced by high IOP or the increased level of pHSP27 is the result of the 4-fold increase in the total HSP27 level. It would be interesting to see if the ratio between pHSP27 and HSP27 is changing in favor of pHSP27 with glaucoma progression. Further research is required to demonstrate the protective role of pHSP27 in glaucomatous retinas. Nevertheless, the fact that HSP27 expression is stimulated in response to high IOP in various retinal cell types experiencing stress once again demonstrates the involvement of HSPs in stress response mechanism and points at its potential role in cell protection.