April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
The neuroprotective protein Stanniocalcin-1 (STC-1) has ocular hypotensive properties in the human anterior segment organ culture model
Author Affiliations & Notes
  • Gavin W Roddy
    Ophthalmology, Mayo Clinic, Rochester, MN
  • Cindy K Bahler
    Ophthalmology, Mayo Clinic, Rochester, MN
  • Bradley H Holman
    Ophthalmology, Mayo Clinic, Rochester, MN
  • Michael P Fautsch
    Ophthalmology, Mayo Clinic, Rochester, MN
  • Footnotes
    Commercial Relationships Gavin Roddy, None; Cindy Bahler, None; Bradley Holman, None; Michael Fautsch, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 559. doi:
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      Gavin W Roddy, Cindy K Bahler, Bradley H Holman, Michael P Fautsch; The neuroprotective protein Stanniocalcin-1 (STC-1) has ocular hypotensive properties in the human anterior segment organ culture model. Invest. Ophthalmol. Vis. Sci. 2014;55(13):559.

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

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Abstract

Purpose: Current therapies for glaucoma lower intraocular pressure but do not provide neuroprotection. STC-1 is a multi-functional protein that has recently been shown to be neuroprotective for photoreceptors and ganglion cells in vivo. In this study, we evaluated the ocular hypotensive properties of STC-1.

Methods: Paired human eyes (n=5) were obtained from the MN Lions Eye Bank. Following bisection of the eyes at the equator and removal of the iris, lens and vitreous, the anterior segments were clamped in a modified petri dish, placed at 37°C in a 5% CO2 atmosphere and perfused with Dulbecco’s Modified Eagle’s Media (DMEM) at the normal human flow rate of 2.5 μl/min. Upon stabilization of baseline IOP, one eye received an anterior chamber exchange with DMEM containing STC-1 (5, 50 or 500 ng/ml) while the fellow eye received an anterior chamber exchange with DMEM alone. Pressures were continuously monitored with a transducer connected to the second access cannula built into the dish and recorded with a custom designed computerized system. Histology was analyzed by transmission electron microscopy and evaluated by masked observation.

Results: All anterior segments perfused with STC-1 at 500 ng/ml had increased outflow facility (0.15 ± 0.03 to 0.27 ± 0.09 µl/min/mmHg, n=5, P=0.02) compared to baseline. In contrast, paired controls treated with vehicle showed no change in outflow facility (0.20 ± 0.03 to 0.20 ± 0.02 µl/min/mmHg, n=5, P=0.76). Anterior segments perfused with STC-1 at 5 ng/ml (0.15 ± 0.04 to 0.15 ± 0.04 µl/min/mmHg, n=2) and 50 ng/ml (0.14 ± 0.05 to 0.18 ± 0.07 µl/min/mmHg, n=4) had no significant effect on outflow facility (P=0.09). Morphological analysis showed similar cell numbers in the trabecular meshwork and Schlemm’s canal. No major disruptions of the juxtacanalicular region or the basement membrane of Schlemm’s canal inner and outer wall were observed.

Conclusions: STC-1 increased outflow facility in the human anterior segment culture model. STC-1 appears to be a novel molecule that can both reduce IOP and provide neuroprotection.

Keywords: 633 outflow: trabecular meshwork • 615 neuroprotection • 420 anterior chamber  
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