December 2002
Volume 43, Issue 13
ARVO Annual Meeting Abstract  |   December 2002
Effect of RGD Peptide on Outflow Facility in Human Anterior Segments in Perfusion Organ Culture
Author Affiliations & Notes
  • CR Hann
    Ophthalmology Mayo Clinic Rochester MN
  • CK Bahler
    Ophthalmology Mayo Clinic Rochester MN
  • MP Fautsch
    Ophthalmology Mayo Clinic Rochester MN
  • DH Johnson
    Ophthalmology Mayo Clinic Rochester MN
  • Footnotes
    Commercial Relationships   C.R. Hann, None; C.K. Bahler, None; M.P. Fautsch, None; D.H. Johnson, None. Grant Identification: Support: NIH Grant EY 07065 and Research to Prevent Blindness, Inc.
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 1024. doi:
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      CR Hann, CK Bahler, MP Fautsch, DH Johnson; Effect of RGD Peptide on Outflow Facility in Human Anterior Segments in Perfusion Organ Culture . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1024.

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

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Abstract: : Purpose: To determine the effect of RGD peptide on outflow facility and histology of the human eye, and to determine whether RGD can cause disruption of trabecular cells in monolayer culture. The RGD sequence is found in fibronectin and other molecules, and is involved in the attachment of cells to extracellular matrix. Methods: Six pairs of anterior segments from normal human eyes were cultured and increasing doses (50-1000 µM) of RGD were added using anterior chamber exchange; RGE was used as a control in fellow eyes. Eyes were fixed and examined by light and electron microscopy. Monolayer trabecular cells were plated for 24 hrs, then RGD or RGE was added at 200 µM or 500 µM. Morphological effects were examined by light microscopy. Results: RGD, at all concentrations, produced minimal pressure changes in perfused anterior segments. Microscopic observation revealed loss of about 30% of Schlemm's canal cells, with the underlying extracellular matrix generally remaining intact. Cell junctions were attenuated and contained gaps. Cells in the JCT and other meshwork regions appeared unaltered with no evidence of loss of attachment to the extracellular matrix or trabecular beams. In monolayer cell culture, RGD showed focal areas of cell retraction and disruption of the monolayer. Conclusion:: RGD did not cause significant changes in outflow facility in the human eye, although it appeared to cause loss of canal cells. This suggests the extracellular matrix is important in regulating outflow facility.

Keywords: 403 extracellular matrix • 444 intraocular pressure • 601 trabecular meshwork 

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