Page 6 - G. Cell differentiation. division. and death

[G. Cell differentiation, division, and death-6]

Diesel particulate matter 2.5 induces inflammation and

mitochondrial impairment via up-regulation of reactive

oxygen species in corneal epithelial cells

Da Hye Kim¹, Hyesook Lee²˙³, Jeong-Hwan Kim⁴, Seh-Kwang Park⁴, Ji-Won Jeong⁵, Mi-Young Kim⁴, Soo-

Wan Nam¹˙⁶, Yung Hyun Choi²˙³˙⁶

¹Department of Smart Bio-Health, Graduate School, Dong-eui University, Busan 47340, Republic of Korea, ²Anti-

Aging Research Center, Dong-eui University, Busan 47340, Republic of Korea, ³Department of Biochemistry,
Dong-eui University College of Korean Medicine, Busan 47227, Republic of Korea, ⁴Research and Development
Department, BGN CARE Co., Ltd., Busan 47195, Republic of Korea, ⁵BGN Eye Clinic, BGN Eye Clinic, Busan

47195, Republic of Korea, ⁶Biomedical Engineering and Biotechnology Major, College of Engineering, Dong-Eui
University, Busan 47340, Republic of Korea

Fine PM is referred to as PM2.5 (particulate matter with a diameter less than 2.5 μm), and several studies have
linked PM2.5 to ocular surface diseases. Nevertheless, the few studies on the biological effect and underlying

mechanism of PM2.5 on the eye have been limited. The aim of this study was to evaluate the biological effect of
PM2.5 on primary rat corneal epithelial cells (RCECs) and to identify the mechanism. The result of gene expression

microarray showed that PM2.5 enhanced the expression of pro-inflammatory mediators, such as cytokines and
chemokines. We also found that up-regulation of the secretion of inflammatory cytokines was accompanied by

activation of NF-κB and phosphorylation of p38 MAPK. It is worth noting that PM2.5 markedly increased intracellular
ROS and suppressed the protein expression of mitophagy regulator, such as PINK, Parkin and Wee1. However, the
inhibition of ROS by N-acetylcysteine significantly suppressed the PM2.5-mediated cellular dysfunction including

expression and secretion of inflammatory mediators, mitochondrial membrane potential loss, DNA damage and NF-

κB activation. In conclusion, our data suggested that PM2.5-induced inflammation and mitochondrial dysfunction
are dependent on the ROS/NF-κB signaling pathway in RCECs.