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Editors Selection IGR 14-3

Basic Research - Outflow: Cochlin effect on aqueous outflow

Comment by Abbot Clark on:

47113 Cochlin induced TREK-1 co-expression and annexin A2 secretion: Role in trabecular meshwork cell elongation and motility, Goel M; Sienkiewicz AE; Picciani R et al., PLoS ONE, 2011; 6: 23070

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Previous work has shown that expression of the extracellular protein cochlin is elevated in the trabecular meshwork (TM) of POAG subjects and that cochlin decreases the outflow facility of perfusion cultured anterior segments. Therefore, cochlin has been implicated in the impaired aqueous humor outflow and elevated IOP associated with POAG. In a recent publication Goel et al. (1157) have attempted to determine the molecular mechanisms that may be responsible for cochlin eff ects on the aqueous outflow pathway. They used multiple normal and glaucoma TM cell strains to investigate the effects of cochlin over-expression on TM cell morphology and mobility, and they show that cochlin induces cell elongation and filopodia formation. Cochlin also induces the expression of TREK-1, a stretch activated channel, and annexin A2, a protein involved in cytoskeletal remodeling. The authors also report that cochlin interacts with TREK-1 and annexin A2. Other proteins including diaphanous related formin-1, α-tectorin, gasdermin, and wolframin were examined and reported to be elevated in glaucoma TM cells, although the relevance of these proteins to their overall hypothesis is unclear. The authors propose that cochlin along with TREK-1 act as mechanosensing and mechanotransduction in TM cells to regulate aqueous humor outflow. However, the authors present no direct evidence to support this hypothesis. How do changes in cell morphology and mobility translate to mechanosensing? In many cases, the data presented showed only a single or a few TM cells. It is not clear how many cells were examined or how many different TM cell strains were tested. For example, the authors conclude that the expression of several proteins is increased in glaucoma TM cells based on a single western immunoblot comparing a single normal and single glaucoma TM cell strain. Their data would be significantly strengthened if they had reported quantitative data along with statistical analyses of their data as well as by inclusion of proper controls for their experiments. The glaucoma community eagerly awaits further clarification on the role and importance of cochlin in the regulation of the aqueous outflow facility.

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