PBX1 attenuates H₂O₂-induced oxidant stress in human trabecular meshwork cells via promoting NANOG-mediated PI3K/AKT signaling pathway.

ABSTRACT: Oxidative stress-induced excessive extracellular matrix (ECM) deposition in trabecular meshwork (TM) tissue is considered the major pathological procedure of glaucoma. This study aimed to explore the role and regulatory mechanism of pre-B-cell leukemia transcription factor 1 (PBX1) in H₂O₂-induced human trabecular meshwork cells (HTMCs). Expressions of PBX1, NANOG, ECM, and pathway-related factors were detected by qRT-PCR and western blot. Cell viability and apoptosis of HTMCs were measured using CCK-8 and flow cytometry assays. Reactive oxygen species (ROS), superoxide dismutase (SOD), and L-glutathione (GSH) levels were detected to evaluate oxidative stress. Through luciferase reporter assay, the association between PBX1 and NANOG was verified. Results presented tha

SUBMITTER: Wang L 

PROVIDER: S-EPMC9672266 | biostudies-literature | 2022 Nov

REPOSITORIES: biostudies-literature