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Editors Selection IGR 15-3

Basic science: Accelerated aging of the trabecular meshworks

Comment by Ernst Tamm on:

12549 Cellular senescence in the glaucomatous outflow pathway, Liton PB; Challa P; Stinnett S et al., Experimental Gerontology, 2005; 40: 745-748

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POAG is a disease that is typically found in elderly patients. As elevated intraocular pressure and increased aqueous humor outflow resistance in POAG result from a progressive failure of the trabecular meshwork, Liton et al. (778) studied the question, if senescent cells might accumulate in the trabecular meshwork of patients with POAG. To this end, they investigated the expression of senescent-associated-β-galactosidase, a well known marker for cellular senescence. The results show an increase in activity of β-galactosidase in the TM of patients with POAG and indicate a significant increase in the number of senescent cells in the outflow pathways of aqueous humor. It seems reasonable to assume that cellular senescence contributes to the malfunction of the trabecular meshwork in POAG and results in an increase in aqueous humor outflow resistance. The question that remains to be answered is, if the increase in activity of senescent-associated-β-galactosidase is involved in the cause of glaucoma, or merely just a symptom of it. A likely scenario could involve the accumulation of senescent cells as side effect due to long-term medical glaucoma therapy. An interesting aspect of this study relates to the fact that the lacZ gene encoding for the enzyme β-galactosidase is quite often used as reporter gene to monitor successful gene transfer after experimental gene therapy. As the protocols to detect senescence-associated-β-galactosidase and β-galactosidase encoded by lacZ are quite similar, researchers (and reviewers) studying gene transfer in the TM should be aware about the strong potential for false positive results in the TM of patients with POAG.

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