Abstract
It has been suggested that common mechanisms may underlie the pathogenesis of primary open-angle glaucoma (POAG) and steroid-induced glaucoma (SIG). The biomechanical properties (stiffness) of the trabecular meshwork (TM) have been shown to differ between POAG patients and unaffected individuals. While features such as ocular hypertension and increased outflow resistance in POAG and SIG have been replicated in mouse models, whether changes of TM stiffness contributes to altered IOP homeostasis remains unknown. We found that outer TM was stiffer than the inner TM and, there was a significant positive correlation between outflow resistance and TM stiffness in mice where conditions are well controlled. This suggests that TM stiffness is intimately involved in establishing outflow resistance, motivating further studies to investigate factors underlying TM biomechanical property regulation. Such factors may play a role in the pathophysiology of ocular hypertension. Additionally, this finding may imply that manipulating TM may be a promising approach to restore normal outflow dynamics in glaucoma. Further, novel technologies are being developed to measure ocular tissue stiffness in situ. Thus, the changes of TM stiffness might be a surrogate marker to help in diagnosing altered conventional outflow pathway function if those technologies could be adapted to TM.
Highlights
Previous studies have indicated that trabecular meshwork (TM) stiffness may be related to aqueous humor outflow resistance[1,2,3,4]
Using atomic force microscopy (AFM), TM stiffness was found to be dramatically increased in human glaucomatous eyes compared to that in normal eyes, which was hypothesized to be associated with dysregulation of the extracellular matrix (ECM) observed in glaucoma[1]
The major finding of this work is that there is a significant correlation between aqueous humor outflow resistance and TM stiffness across two wild-type strains of mice and in DEX-treated mice
Summary
Previous studies have indicated that trabecular meshwork (TM) stiffness may be related to aqueous humor outflow resistance[1,2,3,4]. In normal and glaucomatous human eyes, we have recently reported an association between outflow facility and TM stiffness as deduced by OCT imaging and numerical modeling[4]. SIG has commonalities with primary open-angle glaucoma, and an understanding of TM changes in SIG may shed light on TM dysfunction in glaucoma in general These previous findings relating increased TM stiffness to glaucoma are important and subject to certain limitations. In other studies involving DEX exposure, TM stiffness and outflow resistance were not both measured, so it is not known if these two factors are associated. Mice do not develop POAG as human do, genetically distinct mouse strains have different IOPs, and different conventional outflow facilities[8]. Using different strains of mice may provide one way to study the relation of TM stiffness to IOP and outflow facility
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