Particulate matter 2.5 promotes inflammation and cellular dysfunction <i>via</i> reactive oxygen species/p38 MAPK pathway in primary rat corneal epithelial cells
Da Hye Kim, Hyesook Lee, Hyun Hwangbo, So Young Kim, Seon Yeong Ji, Min Yeong Kim, Seh-Kwang Park, Sung-Ho Park, Mi-Young Kim, Gi‐Young Kim, JaeHun Cheong, Soo‐Wan Nam, Yung Hyun Choi
Abstract
PURPOSE: and identify the toxic mechanism involved. MATERIALS AND METHODS: Primary cultured RCECs were characterized by pan-cytokeratin (CK) staining. In PM2.5-exposed RCECs, cell viability, microarray gene expression, inflammatory cytokine levels, mitochondrial damage, DNA double-strand break, and signalling pathway were investigated. RESULTS: -mediated cellular dysfunctions. CONCLUSIONS: -induced ocular surface disorders.
Topics & Concepts
Reactive oxygen speciesCell biologyp38 mitogen-activated protein kinasesMAPK/ERK pathwayViability assayDNA damageMitochondrial ROSInflammationSignal transductionCytotoxicityChemistryOxidative stressBiologyMolecular biologyCellIn vitroImmunologyBiochemistryDNAAir Quality and Health ImpactsClimate Change and Health ImpactsHeme Oxygenase-1 and Carbon Monoxide