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A. L. Yu, A. Kampik, U. C. Welge-Lussen; Hypoxia/Reoxygenation and TGF-ß2 Increase Hsp27 Expression in Human Optic Nerve Head Astrocytes. Invest. Ophthalmol. Vis. Sci. 2007;48(13):4409.
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Reactive astrocytes in glaucomatous optic nerve changes are characterized by an increased expression of heat shock proteins such as heat shock protein 27 (Hsp27). In the pathogenesis of glaucomatous optic nerve damage, ischemia/reperfusion injury and transforming growth factor beta 2 (TGF-ß2) may play an important role. The goal of the present study was to determine the influence of hypoxia/reoxygenation and TGF-ß2 on the expression of Hsp27 in cultured human astrocytes of the optic nerve head (ONH).
Cultured human astrocytes were incubated under hypoxic conditions (1% O2 for 4 hours) with subsequent reoxygenation (12 to 48 hours). Additionally, cells were treated with 1.0 ng/ml TGF-ß2 for 12 to 48 hours. Expression of Hsp27 was examined by real-time PCR and western-blotting. Levels of TGF-ß2 were analyzed by RT-PCR analysis and ELISA.
Hypoxia/reoxygenation increased the expression of Hsp27 at the mRNA (1.3 to 2 fold) and protein level (1.2 to 1.6 fold). Treatment with 1.0 ng/ml TGF-ß2 for 12 to 48 hours markedly enhanced Hsp27 mRNA approximately 2.8 to 5.1 fold. Using Western blot analysis this increase ranged between 2 to 3 times. TGF-ß2 showed a twofold increase after 12 and 24 hours of reoxygenation at the mRNA and a two- to threefold increase at the protein level.
The process of hypoxia/reoxygenation is capable of inducing the expression of Hsp27 and TGF-ß2 in cultured ONH astrocytes. Therefore, optimization of conditions leading to hypoxia/reoxygenation in the ONH of glaucomatous patients may help to lower the incidence of characteristic changes in the optic nerve.
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