Anti-pollutant effect of oleic acid against urban particulate matter is mediated via regulation of AhR- and TRPV1-mediated signaling in vitro.
Seoyoung ChoiSeyoung YangJi Woong KimKitae KwonSae Woong OhEunbi YuSu Bin HanSoo Hyun KangJung Hyun LeeHeejun HaJeong Kyun YooSu Young KimYoung Soo KimJae Youl ChoChang Seok LeePublished in: Environmental toxicology (2024)
Urban 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.
Keyphrases
- signaling pathway
- particulate matter
- induced apoptosis
- cell proliferation
- oxidative stress
- air pollution
- single cell
- diabetic rats
- pi k akt
- reactive oxygen species
- high glucose
- transcription factor
- neuropathic pain
- immune response
- cell therapy
- machine learning
- stem cells
- cell cycle arrest
- drug induced
- dna methylation
- mesenchymal stem cells
- gene expression
- brain injury
- inflammatory response
- spinal cord
- spinal cord injury
- bone marrow
- dna damage
- electronic health record
- big data
- poor prognosis
- replacement therapy
- living cells
- smoking cessation