Anti‐pollutant effect of oleic acid against urban particulate matter is mediated via regulation of AhR‐ and TRPV1‐mediated signaling in vitro

Author:

Choi Seoyoung1,Yang Seyoung1,Kim Ji Woong2,Kwon Kitae1,Oh Sae Woong1,Yu Eunbi1,Han Su Bin1,Kang Soo Hyun1,Lee Jung Hyun1,Ha Heejun1,Yoo Jeong Kyun2,Kim Su Young2,Kim Young Soo2,Cho Jae Youl3,Lee Jongsung1ORCID

Affiliation:

1. Department of Integrative Biotechnology, Molecular Dermatology Laboratory, College of Biotechnology and Bioengineering Sungkyunkwan University Suwon City Gyunggi Do Korea

2. Materials Science Research Institute LABIO, Inc. Seoul Korea

3. Department of Integrative Biotechnology, Molecular Immunology Laboratory, College of Biotechnology and Bioengineering Sungkyunkwan University Suwon City Gyunggi Do Korea

Abstract

AbstractUrban Particulate Matter (UPM) induces skin aging and inflammatory responses by regulating skin cells through the transient receptor potential vanilloid 1 (TRPV1). Although oleic acid, an unsaturated free fatty acid (FFA), has some functional activities, its effect on UPM‐induced skin damage has not been elucidated. Here, we investigated signaling pathways on how oleic acid is involved in attenuating UPM induced cell damage. UPM treatment increased XRE‐promoter luciferase activity and increased translocation of AhR to the nucleus, resulting in the upregulation of CYP1A1 gene. However, oleic acid treatment attenuated the UPM effects on AhR signaling. Furthermore, while UPM induced activation of TRPV1 and MAPKs signaling which activated the downstream molecules NFκB and AP‐1, these effects were reduced by cotreatment with oleic acid. UPM‐dependent generation of reactive oxygen species (ROS) and reduction of cellular proliferation were also attenuated by the treatment of oleic acid. These data reveal that cell damage induced by UPM treatment occurs through AhR signaling and TRPV1 activation which in turn activates ERK and JNK, ultimately inducing NFκB and AP‐1 activation. These effects were reduced by the cotreatment of oleic acid on HaCaT cells. These suggest that oleic acid reduces UPM‐induced cell damage through inhibiting both the AhR signaling and activation of TRPV1 and its downstream molecules, leading to a reduction of pro‐inflammatory cytokine and recovery of cell proliferation.

Funder

Ministry of Trade, Industry and Energy

Ministry of SMEs and Startups

Publisher

Wiley

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