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Int. J. Mol. Sci. 2018, 19(9), 2660; https://doi.org/10.3390/ijms19092660

Negative Cellular Effects of Urban Particulate Matter on Human Keratinocytes Are Mediated by P38 MAPK and NF-κB-dependent Expression of TRPV 1

1
Molecular Dermatology Laboratory, Department of Integrative Biotechnology, College of Biotechnology and Bioengineering, Sungkyunkwan University, Suwon City, Gyunggi Do 16419, Korea
2
Department of Bio and Chemical Engineering, Hongik University, Sejong City 300-16, Korea
3
AMI Cosmetic Co., Ltd., 19 Yanghwa-ro, Mapo-gu, Seoul 04026, Korea
4
Molecular Immunology Laboratory, Department of Integrative Biotechnology, College of Biotechnology and Bioengineering, Sungkyunkwan University, Suwon City, Gyunggi Do 16419, Korea
5
Biocosmetics Research Center, College of Biotechnology and Bioengineering, Sungkyunkwan University, Suwon City, Gyunggi Do 16419, Korea
These authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Received: 15 August 2018 / Revised: 3 September 2018 / Accepted: 5 September 2018 / Published: 7 September 2018
(This article belongs to the Special Issue Cell Targets and Toxicity)
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Abstract

Urban particulate matter (UPM) exerts negative effects on various human organs. Transient receptor potential vanilloid 1 (TRPV1) is a polymodal sensory transducer that can be activated by multiple noxious stimuli. This study aimed to explore the effects of the UPM 1648a on the expression of TRPV1, and its regulatory mechanisms in HaCaT cells. UPM enhanced TRPV 1 promoter-luciferase reporter activity. UPM also increased expression of the TRPV 1 gene as evidenced by increased mRNA and protein levels of TRPV 1. In addition, elucidation of the underlying mechanism behind the UPM-mediated effects on TRPV 1 expression revealed that UPM can upregulate expression of the TRPV1 gene by activating activator protein-1 (AP-1) and nuclear factor kappa B (NF-κB). The UPM treatment also altered Ca2+ influx and cell proliferation, as well as production of interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β). In addition, these UPM-induced effects were attenuated by SB203580 and ammonium pyrrolidinedithiocarbamate (PDTC). However, SP600125 and PD98059 did not alter the UPM-induced effects. Taken together, these findings indicate that UPM upregulates expression of the TRPV 1 gene, which is mediated by the p38 mitogen-activated protein kinase (MAPK) and NF-κB signaling pathways and suggest that UPM is a potential irritant that can induce skin processes such as aging and inflammatory responses. View Full-Text
Keywords: human keratinocytes; TRPV 1; MAPK; NF-κB; UPM; skin human keratinocytes; TRPV 1; MAPK; NF-κB; UPM; skin
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).
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Kwon, K.; Park, S.-H.; Han, B.S.; Oh, S.W.; Lee, S.E.; Yoo, J.A.; Park, S.J.; Kim, J.; Kim, J.W.; Cho, J.Y.; Lee, J. Negative Cellular Effects of Urban Particulate Matter on Human Keratinocytes Are Mediated by P38 MAPK and NF-κB-dependent Expression of TRPV 1. Int. J. Mol. Sci. 2018, 19, 2660.

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