Overexpression of the inwardly rectifying potassium channel Kir4.1 or Kir4.1 Tyr 9 Asp in Muller cells exerts neuroprotective effects in an experimental glaucoma model.

ABSTRACT: JOURNAL/nrgr/04.03/01300535-202604000-00043/figure1/v/2025-06-30T060627Z/r/image-tiff Downregulation of the inwardly rectifying potassium channel Kir4.1 is a key step for inducing retinal Müller cell activation and interaction with other glial cells, which is involved in retinal ganglion cell apoptosis in glaucoma. Modulation of Kir4.1 expression in Müller cells may therefore be a potential strategy for attenuating retinal ganglion cell damage in glaucoma. In this study, we identified seven predicted phosphorylation sites in Kir4.1 and constructed lentiviral expression systems expressing Kir4.1 mutated at each site to prevent phosphorylation. Following this, we treated Müller glial cells in vitro and in vivo with the mGluR I agonist DHPG to induce Kir4.1 or Kir4.1 Tyr 9 Asp overexpression.

SUBMITTER: Li F 

PROVIDER: S-EPMC12410862 | biostudies-literature | 2026 Apr

REPOSITORIES: biostudies-literature