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Editors Selection IGR 9-2

Basic research: Optic nerve head: Hypoxia

Comment by Elke Lütjen-Drecoll on:

17989 Hypoxia/reoxygenation and TGF-β increase αB-crystallin expression in human optic nerve head astrocytes, Yu AL; Fuchshofer R; Birke M et al., Experimental Eye Research, 2007; 84: 694-706

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Dysregulation of blood circulation leading to hypoxic conditions in the optic nerve head is long discussed to be causative or participating in the inition of PAOG development. One marker for glaucomatous changes in the ONH is increased expression of αB-crystallin, a small stress inducable heat shock protein, by astrocytes. Yu et al. (447) analyzed the effect of hypoxia and subsequent reoxygenation on the expression of αB-crystallin, and on TGF-β-1 and -2 in order to investigate the mechanism of hypoxia/reoxygenation induced αB-crystallin expression.Their results show that hypoxia (4 h, 8 h, 12 h) alone only has a marginal effect on αB-crystallin and TGF-β isoform expression, respectively. Subsequent reoxygenation (12h, 24h) in contrast markedly induced expression of the factors (αB-crystallin 2-3-fold, TGF-β-1/2 2-fold). The authors discuss that during reoxygenation, reactive oxygen species (ROS) accumulate which then activate TGF-β expression.

Mechanistically, hypoxia/reoxygenation causes increased intracellular ROS-levels which induce TGF-β expression which then in turn activates αB-crystallin expression

Treatment with TGF-β-1 and -2 also activated αB-expression to a similar extend (2-fold). Blocking of TGF-β-1/2 by neutralizing antibodies also blocked the hypoxia/reoxygenation mediated αB-crystallin induction. From that the authors concluded that mechanistically, hypoxia/reoxygenation causes increased intracellular ROS-levels which induce TGF-β expression which then in turn activates αB-crystallin expression. This data provides for the first time a possible mode of action by which oxidative stress could contribute to the increase of TGF-β and αB-crystallin observed in the optic nerve of glaucomatous eyes. If this also provides a general mechanism which could explain the elevation of TGF-β or other stress factors in the vitreous or the aqueous humor, respectively, which is also frequently observed in glaucoma, needs to be further elucidated.

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