Regulation of Superoxide by BAP31 through Its Effect on p22^phox and Keap1/Nrf2/HO-1 Signaling Pathway in Microglia.

ABSTRACT: Reactive oxygen species (ROS) production by activation of microglia is considered to be a major cause of neuronal dysfunction, which can lead to damage and death through direct oxidative damage to neuronal macromolecules or derangement of neuronal redox signaling circuits. BAP31, an integral ER membrane protein, has been defined as a regulatory molecule in the CNS. Our latest studies have found that BAP31 deficiency leads to activation of microglia. In this study, we discovered that BAP31 deficiency upregulated LPS-induced superoxide anion production in BV2 cells and mice by upregulating the expression level of p22^phox and by inhibiting the activation of Nrf2-HO-1 signaling. Knockdown of p22^phox/keap1 or use of an NADPH oxidase inhibitor (apocynin) reversed the produc

SUBMITTER: Liu X 

PROVIDER: S-EPMC7969104 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature