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W. Daniel Stamer, Bruce C. Roberts, David L. Epstein; Hydraulic Pressure Stimulates Adenosine 3′,5′-Cyclic Monophosphate Accumulation in Endothelial Cells from Schlemm’s Canal. Invest. Ophthalmol. Vis. Sci. 1999;40(9):1983-1988.
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purpose. Fluid flow across various endothelia results in a variety of
intracellular and extracellular adaptations. In the living eye, aqueous
humor flows across the surface of endothelial cells on trabecular
meshwork (TM) beams and in the juxtacanalicular tissue and through or
between a continuous monolayer of endothelial cells that line
Schlemm’s canal (SC). This study was undertaken to test the hypothesis
that fluid flow induces biochemical changes in the endothelial cells of
the outflow pathway that may modify outflow resistance.
methods. Trabecular meshwork and SC cells isolated from the outflow pathway of
human cadaveric eyes were seeded onto porous filters, placed in
Ussing-type chambers, and subjected to fluid flow driven by a pressure
head of 15 mm Hg on their apical surface. Cell lysates were prepared
and analyzed for adenosine 3′,5′-cyclic monophosphate (cAMP)
accumulation. Barrier function of cell monolayers was examined using
transendothelial electrical resistance measurements.
results. Three different SC cell strains in 14 independent experiments responded
with at least a threefold increase in cAMP that was both time and
pressure dependent. Conversely, flow-treated TM cells failed to respond
in six independent experiments in which five different TM cell strains
were used. Electrical resistance across cell monolayers positively
correlated with cAMP accumulation and was calcium sensitive.
conclusions. cAMP signaling is affected by pressure differentials across SC cell
monolayers and provides evidence for the participation of SC cells in
the regulation of aqueous outflow.
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