Neuronal p58^IPK Protects Retinal Ganglion Cells Independently of Macrophage/Microglia Activation in Ocular Hypertension.

ABSTRACT: p58^IPK is a multifaceted endoplasmic reticulum (ER) chaperone and a regulator of eIF2α kinases involved in a wide range of cellular processes including protein synthesis, ER stress response, and macrophage-mediated inflammation. Systemic deletion of p58^IPK leads to age-related loss of retinal ganglion cells (RGC) and exacerbates RGC damage induced by ischemia/reperfusion and increased intraocular pressure (IOP), suggesting a protective role of p58^IPK in the retina. However, the mechanisms remain elusive. Herein, we investigated the cellular mechanisms underlying the neuroprotection action of p58^IPK using conditional knockout (cKO) mouse lines where p58^IPK is deleted in retinal neurons (Chx10-p58^IPK cKO) or in myeloid cells (

SUBMITTER: McLaughlin T 

PROVIDER: S-EPMC10297187 | biostudies-literature | 2023 Jun

REPOSITORIES: biostudies-literature