TRPV4 and TRPC1 channels mediate the response to tensile strain in mouse Muller cells.

ABSTRACT: Müller glia, a pillar of metabolic, volume regulatory and immune/inflammatory signaling in the mammalian retina, are among the earliest responders to mechanical stressors in the eye. Ocular trauma, edema, detachment and glaucoma evoke early inflammatory activation of Müller cells yet the identity of their mechanotransducers and signaling mechanisms downstream remains unknown. Here, we investigate expression of genes that encode putative stretch-activated calcium channels (SACs) in mouse Müller cells and study their responses to dynamical tensile loading in cells loaded with a calcium indicator dye. Transcript levels in purified glia were Trpc1>Piezo1>Trpv2>Trpv4>>Trpv1>Trpa1. Cyclic radial deformation of matrix-coated substrates produced dose-dependent increases in [Ca²⁺]_i<

SUBMITTER: Jo AO 

PROVIDER: S-EPMC9119919 | biostudies-literature | 2022 Jun

REPOSITORIES: biostudies-literature