April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
Mechanosensitivity of Schlemm’s canal endothelial cells from normal and glaucomatous eyes
Author Affiliations & Notes
  • Enhua H Zhou
    Environmental Health, Harvard School of Public Health, Boston, MA
  • Rudolf Fuchshofer
    Institute of Human Anatomy and Embryology, University of Regensburg, Regensburg, Germany
  • W Daniel Stamer
    Duke Eye Center, Duke University School of Medicine, Durham, NC
  • Quynh N Dang
    Environmental Health, Harvard School of Public Health, Boston, MA
  • Jae H Kim
    Environmental Health, Harvard School of Public Health, Boston, MA
  • Kristin Marie Perkumas
    Duke Eye Center, Duke University School of Medicine, Durham, NC
  • Mark Johnson
    Biomedical Engineering and Ophthalmology, Northwestern University, Evanston, IL
  • Jeffrey J Fredberg
    Environmental Health, Harvard School of Public Health, Boston, MA
  • Footnotes
    Commercial Relationships Enhua Zhou, None; Rudolf Fuchshofer, None; W Daniel Stamer, None; Quynh Dang, None; Jae Kim, None; Kristin Perkumas, None; Mark Johnson, None; Jeffrey Fredberg, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 5684. doi:
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      Enhua H Zhou, Rudolf Fuchshofer, W Daniel Stamer, Quynh N Dang, Jae H Kim, Kristin Marie Perkumas, Mark Johnson, Jeffrey J Fredberg; Mechanosensitivity of Schlemm’s canal endothelial cells from normal and glaucomatous eyes. Invest. Ophthalmol. Vis. Sci. 2014;55(13):5684.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: The aqueous humor mainly flows through the trabecular meshwork (TM) and across the Schlemm’s canal (SC) endothelium. In primary open angle glaucoma (POAG) eyes, resistance to flow increases and TM tissues are 20 times stiffer than that in normal eyes (Last et al. 2011, IOVS. DOI:10.1167). The extent to which elevated tissue stiffness influences SC cells is poorly understood (Zhou et al. 2012, J Royal Society, Interface. DOI: 10.1098). The goal of the current study is to evaluate changes in cell stiffness and gene expression of SC cells induced by stiffened ECM substrate and to compare the responses of normal to glaucomatous SC cells.

Methods: To mimic the spectrum of ECM stiffness from normal TM to glaucomatous TM, we casted polyacrylamide gels with 5 different crosslinker concentrations. Gels were coated with collagen I and seeded with SC cells isolated from normal (n=5) or glaucomatous (n=5) human donor eyes. To measure the stiffness of confluently plated SC cells, we used optical magnetic twisting cytometry (OMTC). The expression levels of 10 genes were examined, including connective tissue growth factor (CTGF), tissue growth factor (TGF-β2), MMP2, SPARC and collagen (col1A1), using real time quantitative PCR.

Results: Cell stiffness increased with increasing substrate stiffness for both normal and glaucomatous SC cells. This increase in cell stiffness was significantly greater for glaucomatous SC cells than for normals (p = 0.02). CTGF, MMP2, SPARC and col1A1 all exhibited significantly increased expression level with increased substrate stiffness (p<0.05) with expression increased by up to 18 fold (col1A1). The increase in CTGF expression with increasing substrate stiffness was significantly greater in glaucomatous SC cells (11.3 fold) than in normals (3.9 fold) (p < 0.05). The average expression level of CTGF was also higher in glaucomatous SC cells.

Conclusions: Elevated substrate stiffness led to increases in SC cell stiffness and in ECM-related gene expression, both of which known to be associated with elevated outflow resistance. Importantly, glaucomatous SC cells were significantly more responsive to substrate stiffness as compared to controls. Mechanosensitivity of SC cells represents a therapeutic target for restoring the function of the conventional outflow pathway.

Keywords: 633 outflow: trabecular meshwork • 493 cytoskeleton • 568 intraocular pressure  
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