Pressure-dependent Modulation of Inward-Rectifying K+ Channels: Implications for Cation Homeostasis and K+ Dynamics in Glaucoma.

Pressure-dependent Modulation of Inward-Rectifying K+ Channels: Implications for Cation Homeostasis and K+ Dynamics in Glaucoma. Am J Physiol Cell Physiol. 2019 Jun 05;: Authors: Fischer RA, Roux AL, Wareham L, Sappington RM Abstract Glaucoma is a leading cause of blindness worldwide, resulting from degeneration retinal ganglion cells (RGCs), which form the optic nerve. Prior to structural degeneration, RGCs exhibit physiological deficits. Müller glia provide homeostatic regulation of ions that supports RGC physiology through a process called K+ siphoning. Recent studies suggest that several retinal conditions, including glaucoma, involve changes in the expression of K+ channels in Müller glia. To clarify whether glaucoma-related stressors directly alter expression and function of K+ channels in Müller glia, we examined changes in the expression of inwardly rectifying K+ (Kir) channels and two-pore domain (K2P) channels in response to elevated intraocular pressure (IOP) in vivo and in vitro in primary cultures of Müller glia exposed to elevated hydrostatic pressure. We then measured outcomes of cell health, cation homeostasis and cation flux in Müller glia cultures. Transcriptome analysis in a murine model of microbead-induced glaucoma revealed pressure-dependent downregulation of Kir and K2P channels in vivo. Changes in the expression and localization of Kir and K2P channels in response to elevated pressure were also found in M...
Source: Am J Physiol Cell Ph... - Category: Cytology Authors: Tags: Am J Physiol Cell Physiol Source Type: research