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Michael P. Fautsch, Cindy K. Bahler, David J. Jewison, Douglas H. Johnson; Recombinant TIGR/MYOC Increases Outflow Resistance in the Human Anterior Segment. Invest. Ophthalmol. Vis. Sci. 2000;41(13):4163-4168.
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purpose. To determine the effect of human recombinant TIGR/myocilin (MYOC)
protein on outflow resistance in the human anterior segment.
methods. A cDNA for MYOC was inserted into a bacterial expression system and
purified with nickel ion affinity chromatography. The anterior segments
of 12 pairs of human eyes were placed in perfusion organ culture. One
eye received an anterior chamber exchange with partially purified
recombinant MYOC (25 μg), whereas the other eye received either
heat-denatured recombinant MYOC (25 μg), partially purifiedβ
-galactosidase (25 or 250 μg), or partially purified control
proteins isolated from a null expression lysate (25 μg). Eyes were
fixed up to 72 hours after infusion, and immunohistochemistry was
performed using anti-MYOC polyclonal antibody.
results. Recombinant MYOC caused an increase in IOP over 12 hours, increasing
outflow resistance 94%, whereas the fellow eye infused with null
expression sample increased 12% (n = 7; P = 0.0005). When compared with recombinant MYOC,
neither heat-denatured MYOC, recombinant β-galactosidase, bovine
serum albumin, nor fetal calf serum caused an increase in outflow
resistance. MYOC IOP remained above baseline levels for 48 to 72 hours.
Immunohistochemistry results confirmed the presence of recombinant MYOC
in the trabecular meshwork.
conclusions. Recombinant MYOC increased outflow resistance in human anterior
segments, whereas control proteins did not. MYOC may increase outflow
resistance by specific interactions within the trabecular
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