期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 22, 期 20, 页码 -出版社
MDPI
DOI: 10.3390/ijms222010941
关键词
2-IPMA; primary cilia; dermal fibroblasts; oxidative stress; inflammation
资金
- National Research Foundation of Korea - Ministry of Science ICT [2020R1A2C2003523]
- Ministry of Education [2020R1I1A1A01074053]
- AMOREPACIFIC Corporation
- National Research Foundation of Korea [2020R1A2C2003523] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
2-Isopropylmalic acid (2-IPMA) promotes primary ciliogenesis in dermal fibroblasts, ameliorating PM2.5-induced inflammation. Additionally, 2-IPMA inhibits oxidative stress and inflammatory response caused by PM2.5.
Particulate matters (PMs) increase oxidative stress and inflammatory response in different tissues. PMs disrupt the formation of primary cilia in various skin cells, including keratinocytes and melanocytes. In this study, we found that 2-isopropylmalic acid (2-IPMA) promoted primary ciliogenesis and restored the PM2.5-induced dysgenesis of primary cilia in dermal fibroblasts. Moreover, 2-IPMA inhibited the generation of excessive reactive oxygen species and the activation of stress kinase in PM2.5-treated dermal fibroblasts. Further, 2-IPMA inhibited the production of pro-inflammatory cytokines, including IL-6 and TNF-alpha, which were upregulated by PM2.5. However, the inhibition of primary ciliogenesis by IFT88 depletion reversed the downregulated cytokines by 2-IPMA. Moreover, we found that PM2.5 treatment increased the MMP-1 expression in dermal fibroblasts and a human 3-D-skin model. The reduced MMP-1 expression by 2-IPMA was further reversed by IFT88 depletion in PM2.5-treated dermal fibroblasts. These findings suggest that 2-IPMA ameliorates PM2.5-induced inflammation by promoting primary ciliogenesis in dermal fibroblasts.
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