期刊
MOLECULES
卷 26, 期 17, 页码 -出版社
MDPI
DOI: 10.3390/molecules26175409
关键词
primary cilia; 2-IPMA; particulate matter (PM2; 5); inflammation; RPE cells
资金
- National Research Foundation of Korea - Ministry of Science ICT [2020R1A2C2003523, 2020R1A4A1018280]
- Ministry of Education [NRF-2020R1I1A1A01074053]
- National Research Foundation of Korea [2020R1A4A1018280, 2020R1A2C2003523] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Dysregulation of primary cilia is associated with various diseases, and 2-IPMA can alleviate PM2.5-induced inflammation by promoting primary ciliogenesis.
Primary cilia mediate the interactions between cells and external stresses. Thus, dysregulation of primary cilia is implicated in various ciliopathies, e.g., degeneration of the retina caused by dysregulation of the photoreceptor primary cilium. Particulate matter (PM) can cause epithelium injury and endothelial dysfunction by increasing oxidative stress and inflammatory responses. Previously, we showed that PM disrupts the formation of primary cilia in retinal pigment epithelium (RPE) cells. In the present study, we identified 2-isopropylmalic acid (2-IPMA) as a novel inducer of primary ciliogenesis from a metabolite library screening. Both ciliated cells and primary cilium length were increased in 2-IPMA-treated RPE cells. Notably, 2-IPMA strongly promoted primary ciliogenesis and restored PM2.5-induced dysgenesis of primary cilia in RPE cells. Both excessive reactive oxygen species (ROS) generation and activation of a stress kinase, JNK, by PM2.5 were reduced by 2-IPMA. Moreover, 2-IPMA inhibited proinflammatory cytokine production, i.e., IL-6 and TNF-alpha, induced by PM2.5 in RPE cells. Taken together, our data suggest that 2-IPMA ameliorates PM2.5-induced inflammation by promoting primary ciliogenesis in RPE cells.
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