May 2006
Volume 47, Issue 13
ARVO Annual Meeting Abstract  |   May 2006
Purinergic Modulation of Human Trabecular Meshwork Cells
Author Affiliations & Notes
  • M.O. Karl
    Department of Biological Structure, University of Washington, Seattle, WA
  • K. Peterson–Yantorno
    Department of Physiology & Medicine, University of Pennsylvania, Philadelphia, PA
  • M.M. Civan
    Department of Physiology & Medicine, University of Pennsylvania, Philadelphia, PA
  • Footnotes
    Commercial Relationships  M.O. Karl, None; K. Peterson–Yantorno, None; M.M. Civan, None.
  • Footnotes
    Support  NIH research grant EY013624; core grant EY01583; M.O. Karl supported by the Herbert Funke Foundation
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 2914. doi:
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      M.O. Karl, K. Peterson–Yantorno, M.M. Civan; Purinergic Modulation of Human Trabecular Meshwork Cells . Invest. Ophthalmol. Vis. Sci. 2006;47(13):2914.

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

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Purpose: : Activation of A1 and A2A subtype adenosine receptors (AR) likely exert opposing effects on outflow of aqueous humor, and thereby, on intraocular pressure. Selective agonists of adenosine receptor (AR) subtypes have previously been applied to trabecular meshwork (TM) and Schlemm's canal (SC) cells to identify the site(s) of differential purinergic modulation. However, the apparent changes in volume monitored by measuring projected cell area might have partially reflected cell contraction and relaxation. In addition, whole–cell current responses of the TM cells previously described were highly variable following application of selective A1, A2A and A3 agonists. The complexity of the electrophysiologic responses may have reflected cell heterogeneity of the populations harvested from collagenase digestion of TM explants.

Methods: : We now report measurements of TM–cell volume using calcein fluorescence quenching, an approach independent of contractile state. Furthermore, we have applied selective AR agonists to a uniform population of human TM cells, the hTM5 cell line.

Results: : A1, but not A2A or A3, AR agonists triggered TM–cell shrinkage. Both A1 and A2A AR agonists produced reproducible increases in TM–cell whole–cell current of similar magnitude.

Conclusions: : The results suggest that previous measurements of explant–derived TM cells may have reflected a range of responses from phenotypically different cell populations, and that the opposing effects of A1 and A2A agonists on outflow resistance are not likely to be mediated by actions on a single population of TM cells.

Keywords: trabecular meshwork • electrophysiology: non-clinical • signal transduction: pharmacology/physiology 

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