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Editors Selection IGR 8-1
Basic Research: Effects glucocorticoid in TM cells
Comment by Abbot Clark on:
25853 Dexamethasone disrupts intercellular junction formation and cytoskeleton organization in human trabecular meshwork cells, Zhuo YH; He Y; Leung KW et al., Molecular Vision, 2010; 16; 61-71
The fact that certain individuals develop ocular hypertension and iatrogenic open-angle glaucoma after glucocorticoid (GC) therapy has been recognized for almost 60 years. Although the resultant IOP elevation and GC-induced glaucoma is due to compromised aqueous humor outflow, the molecular basis for this steroid response is still unclear. GCs induce a plethora of effects on the trabecular meshwork (TM), including altering gene expression, the extracellular matrix, the cytoskeleton, and TM cell functions. Zhuo et al. (574) recently reported the effects of the potent GC dexamethasone on the actin cytoskeleton as well as junctional proteins ZO-1 and connexin 43 (Cx43) in cultured human TM cells. Interestingly, the authors did not find a GC-induced change in TM cell shape and increase in cell size, which has previously been reported by other investigators.
The combined effects of GCs on the TM cell cytoskeleton, junctional complexes between cells, and extracellular matrix likely play an important role regulating TM cell function and aqueous outflow through the TM
They did find that GC treatment increased ZO-1 and Cx43 expression suggesting GC-mediated effects on tight and gap junctions, in agreement with previous reports. The authors also showed that GCs reorganize the actin cytoskeleton to form microfilament tangles and cross-linked actin networks, which have been previously reported by other groups. Interestingly, similar cytoskeletal changes occurred in GTM cells, which were even more responsive to the cytoskeletal effects of GCs, again in agreement with previous publications. The combined effects of GCs on the TM cell cytoskeleton, junctional complexes between cells, and extracellular matrix (shown by others) likely play an important role regulating TM cell function and aqueous outflow through the TM. Since POAG patients are more responsive to GC and steroid responders are more likely to develop POAG, studies like this on the molecular effects of GCs on the TM will ultimately provide a better understanding of POAG.
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