Changes to zonular tension alters the subcellular distribution of AQP5 in regions of influx and efflux of water in the rat lens

Abstract

<jats:title>ABSTRACT</jats:title><jats:sec><jats:title>Purpose</jats:title><jats:p>The lens utilizes circulating fluxes of ions and water that enter the lens at both poles and exit at the equator to maintain its optical properties. We have mapped the subcellular distribution of the lens aquaporins (AQP0, 1, &amp; 5) in these water influx and efflux zones and investigated how their membrane location is affected by changes in tension applied to the lens by the zonules.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Immunohistochemistry using AQP antibodies was performed on axial sections obtained from rat lenses that had been removed from the eye and then fixed, or were fixed <jats:italic>in situ</jats:italic> to maintain zonular tension. Zonular tension was pharmacologically modulated by applying either tropicamide (increased), or pilocarpine (decreased). AQP labelling was visualized using confocal microscopy.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Modulation of zonular tension had no effect on AQP1 or AQP0 labelling in either the water efflux, or influx zones. In contrast, AQP5 labelling changed from membranous to cytoplasmic in response to both mechanical and pharmacologically induced reductions in zonular tension in both the efflux zone, and anterior (but not posterior) influx zone associated with the lens sutures.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>Altering zonular tension dynamically regulates the membrane trafficking of AQP5 in the efflux and anterior influx zones to potentially change the magnitude of circulating water fluxes in the lens.</jats:p></jats:sec>

Lens aquaporin-5 inserts into bovine fiber cell plasma membranes through mitochondria-associated lysosome secretion

“…Results from bafilomycin A1 treatment also provide further evidence that AQP5 functions as a regulatory water channel whose trafficking is inducible in the mammalian lens. Petrova et al has previously demonstrated dynamic AQP5 subcellular localization changes in response to changes in zonular tension via mechanosensitive TRPV1 channel agonism 17,21 . Since AQP5 plasma membrane insertion significantly increases fiber cell water permeability in both mouse and rat lenses 17 , regulation of AQP5 subcellular localization can alter lens water homeostasis.…”

“…The important role of AQP5 in maintaining lens homeostasis is implied by its expression in all mammalian lenses studied to date including human 12,[18][19][20] , bovine 12 , mouse 11,12,16,17,[19][20][21] , rat 12,17,21 , rabbit 8 , and dog 22 lenses. Functional studies demonstrate the relationship between AQP5 expression and lens osmotic homeostasis.…”

“…Immunohistochemical studies show AQP5 primarily localized to the plasma membrane in the fiber cells of the mouse lens cortex and to cytoplasmic vesicles in the rat lens cortex and the extent of fiber cell permeability correlates to plasma membrane AQP5 abundance 17 . Cytoplasmic AQP5 in rat lenses is dynamically inserted into fiber cell plasma membranes in response to changes in zonular tension and thereby increases fiber cell plasma membrane water permeability (P H2O ) 17,21 .…”

Effect of Alpha-Glucosyl-Hesperidin Consumption on Lens Sclerosis and Presbyopia

“…It has also been reported that oral treatment with Hsd ameliorated lens fluid influx and osmotic imbalance in diabetic cataract lenses [ 25 ]. Membrane insertion of TRPV4 and AQP5 was observed in response to accommodation changes [ 10 , 11 ]. As fiber cells differentiate, they lose their cellular organelles and their ability to perform de novo protein synthesis [ 26 , 27 ].…”

“…Among the AQP family, AQP0, AQP1, and AQP5 are expressed in lens cells. It was reported that the distribution of TRPV4 in the peripheral fiber cells and AQP5 in the efflux and anterior influx zones altered their subcellular localization in response to mechanical and pharmacologically induced reductions in zonular tension [ 10 , 11 ]. These data suggest that AQPs and TRPVs could exist as a store of channels that could be recruited to the plasma membrane to control the water circulation and intracellular pressure in the lens.…”