ArticleBiomechanics and modeling in mechanobiology2015
Finite element analysis of the pressure-induced deformation of Schlemm's canal endothelial cells.
Article in Biomechanics and modeling in mechanobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- Increased stiffness and flow resistance of the inner wall of Schlemm's canal in glaucomatous human eyes.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Transport across Schlemm's canal endothelium and the blood-aqueous barrier.Experimental eye research · 2016Review
- A Closer Look at Schlemm's Canal Cell Physiology: Implications for Biomimetics.Journal of functional biomaterials · 2015Review
- Glaucoma Genes and Mechanisms.Progress in molecular biology and translational science · 2015Review
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
The endothelial cells lining the inner wall of Schlemm's canal (SC) in the eye are relatively unique in that they support a basal-to-apical pressure gradient that causes these cells to deform, creating giant vacuoles and transendothelial pores through which the aqueous humor flows. Glaucoma is associated with an increased resistance to this flow. We used finite element modeling and estimates of cell modulus made using atomic force microscopy to characterize the pressure-induced deformation of SC cells and to estimate the maximum pressure drop that SC cells can support. We examined the effects of cell geometry, cell stiffness, and the contribution of the cell cortex to support the pressure-generated load. We found that the maximum strain generated by this loading occurs at the points of cell-substrate attachment and that the cortex of the cells bears nearly all of this load. The ability of these cells to support a significant transcellular pressure drop is extremely limited (on the order of 5 mmHg or less) unless these cells either stiffen very considerably with increasing deformation or have substantial attachments to their substratum away from their periphery. This puts limits on the flow resistance that this layer can generate, which has implications regarding the site where the bulk of the flow resistance is generated in healthy and glaucomatous eyes.
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