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.
journal_name
Biomech Model Mechanobioljournal_title
Biomechanics and modeling in mechanobiologyauthors
Vargas-Pinto R,Lai J,Gong H,Ethier CR,Johnson Mdoi
10.1007/s10237-014-0640-2subject
Has Abstractpub_date
2015-08-01 00:00:00pages
851-63issue
4eissn
1617-7959issn
1617-7940journal_volume
14pub_type
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