Specialized pro-resolving mediator 7S MaR1 inhibits IL-6 expression via modulating ROS/p38/ERK/NF-κB pathways in PM10-exposed keratinocytes

Keratinocytes are susceptible to airborne particulate matter (PM) exposure, resulting in human skin barrier dysfunction. Therefore, it is important to find useful reagents to resolve skin damages caused by PM. Here, we explored the protective effect of 7S MaR1, a specialized pro-resolving mediator d...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:BMB reports 2024-11, Vol.57 (11), p.490-496
Hauptverfasser: Kim, Jinju, Park, Hyo-Min, Lim, Chae-Min, Jeon, Kyeong-Bae, Kim, Seonhwa, Lee, Jin, Hong, Jin-Tae, Oh, Deok-Kun, Yang, Young, Yoon, Do-Young
Format: Artikel
Sprache:eng
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 496
container_issue 11
container_start_page 490
container_title BMB reports
container_volume 57
creator Kim, Jinju
Park, Hyo-Min
Lim, Chae-Min
Jeon, Kyeong-Bae
Kim, Seonhwa
Lee, Jin
Hong, Jin-Tae
Oh, Deok-Kun
Yang, Young
Yoon, Do-Young
description Keratinocytes are susceptible to airborne particulate matter (PM) exposure, resulting in human skin barrier dysfunction. Therefore, it is important to find useful reagents to resolve skin damages caused by PM. Here, we explored the protective effect of 7S MaR1, a specialized pro-resolving mediator derived from docosahexaenoic acid, on skin inflammation and the oxidative stress induced by PM with a diameter 10 μm or less (PM10) in human keratinocyte HaCaT cells. Interestingly, PM10-induced ROS generation was modulated by 7S MaR1 via the recovery of ROS scavenger genes. 7S MaR1 reduced PM10-induced IL-6 expression via modulating the p38/ERK/NF-κB signaling pathways. These results demonstrate that PM10 induces inflammatory cytokines, which can lead to skin diseases. In addition, 7S MaR1 can resolve inflammation caused by PM10-induced oxidative stress and inflammatory cytokines. [BMB Reports 2024; 57(11): 490-496].Keratinocytes are susceptible to airborne particulate matter (PM) exposure, resulting in human skin barrier dysfunction. Therefore, it is important to find useful reagents to resolve skin damages caused by PM. Here, we explored the protective effect of 7S MaR1, a specialized pro-resolving mediator derived from docosahexaenoic acid, on skin inflammation and the oxidative stress induced by PM with a diameter 10 μm or less (PM10) in human keratinocyte HaCaT cells. Interestingly, PM10-induced ROS generation was modulated by 7S MaR1 via the recovery of ROS scavenger genes. 7S MaR1 reduced PM10-induced IL-6 expression via modulating the p38/ERK/NF-κB signaling pathways. These results demonstrate that PM10 induces inflammatory cytokines, which can lead to skin diseases. In addition, 7S MaR1 can resolve inflammation caused by PM10-induced oxidative stress and inflammatory cytokines. [BMB Reports 2024; 57(11): 490-496].
doi_str_mv 10.5483/BMBRep.2024-0124
format Article
fullrecord <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_11608853</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3115095849</sourcerecordid><originalsourceid>FETCH-LOGICAL-p174t-a179977daabf10dd955ea8954d6d9aae6c1913ef6d50ea52f8c744521f7035233</originalsourceid><addsrcrecordid>eNpVj01OwzAQRiMEEgjYs_SSjakdx3G8QhTxJ1qKWpDYRdN4Qi3S2MRpoZyBE3EIzkQquoDVjPTNe58mio44O5FJJnr9YX-M_iRmcUIZj5OtaI9rldJUsaftP_tudBiCnTIphEpVpveiz4nHwkJlP9AQ3zjaYHDV0tbPZI7GQusaoiZkCGNObD2zU9sGcjOgKcF3390G62qytEDmziwqaNfgeDTpeZH1Lsa3vbtL-v3VJx7a2RusQucg90POaEe70FW-YLOGXLFqMRxEOyVUAQ83cz96vLx4OL-mg9HVzfnZgHqukpYCV1orZQCmJWfGaCkRMi0TkxoNgGnBNRdYpkYyBBmXWaGSRMa8VEzIWIj96PTX6xfT7ssC67aBKveNnUOzyh3Y_H9S21n-7JY55ynLMrk2HG8MjXtdYGjzuQ0FVhXU6BYhF5xLpmWWaPEDc7iBPw</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>3115095849</pqid></control><display><type>article</type><title>Specialized pro-resolving mediator 7S MaR1 inhibits IL-6 expression via modulating ROS/p38/ERK/NF-κB pathways in PM10-exposed keratinocytes</title><source>PubMed (Medline)</source><source>Alma/SFX Local Collection</source><source>Free Full-Text Journals in Chemistry</source><creator>Kim, Jinju ; Park, Hyo-Min ; Lim, Chae-Min ; Jeon, Kyeong-Bae ; Kim, Seonhwa ; Lee, Jin ; Hong, Jin-Tae ; Oh, Deok-Kun ; Yang, Young ; Yoon, Do-Young</creator><creatorcontrib>Kim, Jinju ; Park, Hyo-Min ; Lim, Chae-Min ; Jeon, Kyeong-Bae ; Kim, Seonhwa ; Lee, Jin ; Hong, Jin-Tae ; Oh, Deok-Kun ; Yang, Young ; Yoon, Do-Young</creatorcontrib><description>Keratinocytes are susceptible to airborne particulate matter (PM) exposure, resulting in human skin barrier dysfunction. Therefore, it is important to find useful reagents to resolve skin damages caused by PM. Here, we explored the protective effect of 7S MaR1, a specialized pro-resolving mediator derived from docosahexaenoic acid, on skin inflammation and the oxidative stress induced by PM with a diameter 10 μm or less (PM10) in human keratinocyte HaCaT cells. Interestingly, PM10-induced ROS generation was modulated by 7S MaR1 via the recovery of ROS scavenger genes. 7S MaR1 reduced PM10-induced IL-6 expression via modulating the p38/ERK/NF-κB signaling pathways. These results demonstrate that PM10 induces inflammatory cytokines, which can lead to skin diseases. In addition, 7S MaR1 can resolve inflammation caused by PM10-induced oxidative stress and inflammatory cytokines. [BMB Reports 2024; 57(11): 490-496].Keratinocytes are susceptible to airborne particulate matter (PM) exposure, resulting in human skin barrier dysfunction. Therefore, it is important to find useful reagents to resolve skin damages caused by PM. Here, we explored the protective effect of 7S MaR1, a specialized pro-resolving mediator derived from docosahexaenoic acid, on skin inflammation and the oxidative stress induced by PM with a diameter 10 μm or less (PM10) in human keratinocyte HaCaT cells. Interestingly, PM10-induced ROS generation was modulated by 7S MaR1 via the recovery of ROS scavenger genes. 7S MaR1 reduced PM10-induced IL-6 expression via modulating the p38/ERK/NF-κB signaling pathways. These results demonstrate that PM10 induces inflammatory cytokines, which can lead to skin diseases. In addition, 7S MaR1 can resolve inflammation caused by PM10-induced oxidative stress and inflammatory cytokines. [BMB Reports 2024; 57(11): 490-496].</description><identifier>ISSN: 1976-670X</identifier><identifier>ISSN: 1976-6696</identifier><identifier>EISSN: 1976-670X</identifier><identifier>DOI: 10.5483/BMBRep.2024-0124</identifier><language>eng</language><publisher>Korean Society for Biochemistry and Molecular Biology</publisher><ispartof>BMB reports, 2024-11, Vol.57 (11), p.490-496</ispartof><rights>Copyright © 2024 by the The Korean Society for Biochemistry and Molecular Biology 2024</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11608853/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11608853/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids></links><search><creatorcontrib>Kim, Jinju</creatorcontrib><creatorcontrib>Park, Hyo-Min</creatorcontrib><creatorcontrib>Lim, Chae-Min</creatorcontrib><creatorcontrib>Jeon, Kyeong-Bae</creatorcontrib><creatorcontrib>Kim, Seonhwa</creatorcontrib><creatorcontrib>Lee, Jin</creatorcontrib><creatorcontrib>Hong, Jin-Tae</creatorcontrib><creatorcontrib>Oh, Deok-Kun</creatorcontrib><creatorcontrib>Yang, Young</creatorcontrib><creatorcontrib>Yoon, Do-Young</creatorcontrib><title>Specialized pro-resolving mediator 7S MaR1 inhibits IL-6 expression via modulating ROS/p38/ERK/NF-κB pathways in PM10-exposed keratinocytes</title><title>BMB reports</title><description>Keratinocytes are susceptible to airborne particulate matter (PM) exposure, resulting in human skin barrier dysfunction. Therefore, it is important to find useful reagents to resolve skin damages caused by PM. Here, we explored the protective effect of 7S MaR1, a specialized pro-resolving mediator derived from docosahexaenoic acid, on skin inflammation and the oxidative stress induced by PM with a diameter 10 μm or less (PM10) in human keratinocyte HaCaT cells. Interestingly, PM10-induced ROS generation was modulated by 7S MaR1 via the recovery of ROS scavenger genes. 7S MaR1 reduced PM10-induced IL-6 expression via modulating the p38/ERK/NF-κB signaling pathways. These results demonstrate that PM10 induces inflammatory cytokines, which can lead to skin diseases. In addition, 7S MaR1 can resolve inflammation caused by PM10-induced oxidative stress and inflammatory cytokines. [BMB Reports 2024; 57(11): 490-496].Keratinocytes are susceptible to airborne particulate matter (PM) exposure, resulting in human skin barrier dysfunction. Therefore, it is important to find useful reagents to resolve skin damages caused by PM. Here, we explored the protective effect of 7S MaR1, a specialized pro-resolving mediator derived from docosahexaenoic acid, on skin inflammation and the oxidative stress induced by PM with a diameter 10 μm or less (PM10) in human keratinocyte HaCaT cells. Interestingly, PM10-induced ROS generation was modulated by 7S MaR1 via the recovery of ROS scavenger genes. 7S MaR1 reduced PM10-induced IL-6 expression via modulating the p38/ERK/NF-κB signaling pathways. These results demonstrate that PM10 induces inflammatory cytokines, which can lead to skin diseases. In addition, 7S MaR1 can resolve inflammation caused by PM10-induced oxidative stress and inflammatory cytokines. [BMB Reports 2024; 57(11): 490-496].</description><issn>1976-670X</issn><issn>1976-6696</issn><issn>1976-670X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNpVj01OwzAQRiMEEgjYs_SSjakdx3G8QhTxJ1qKWpDYRdN4Qi3S2MRpoZyBE3EIzkQquoDVjPTNe58mio44O5FJJnr9YX-M_iRmcUIZj5OtaI9rldJUsaftP_tudBiCnTIphEpVpveiz4nHwkJlP9AQ3zjaYHDV0tbPZI7GQusaoiZkCGNObD2zU9sGcjOgKcF3390G62qytEDmziwqaNfgeDTpeZH1Lsa3vbtL-v3VJx7a2RusQucg90POaEe70FW-YLOGXLFqMRxEOyVUAQ83cz96vLx4OL-mg9HVzfnZgHqukpYCV1orZQCmJWfGaCkRMi0TkxoNgGnBNRdYpkYyBBmXWaGSRMa8VEzIWIj96PTX6xfT7ssC67aBKveNnUOzyh3Y_H9S21n-7JY55ynLMrk2HG8MjXtdYGjzuQ0FVhXU6BYhF5xLpmWWaPEDc7iBPw</recordid><startdate>20241101</startdate><enddate>20241101</enddate><creator>Kim, Jinju</creator><creator>Park, Hyo-Min</creator><creator>Lim, Chae-Min</creator><creator>Jeon, Kyeong-Bae</creator><creator>Kim, Seonhwa</creator><creator>Lee, Jin</creator><creator>Hong, Jin-Tae</creator><creator>Oh, Deok-Kun</creator><creator>Yang, Young</creator><creator>Yoon, Do-Young</creator><general>Korean Society for Biochemistry and Molecular Biology</general><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20241101</creationdate><title>Specialized pro-resolving mediator 7S MaR1 inhibits IL-6 expression via modulating ROS/p38/ERK/NF-κB pathways in PM10-exposed keratinocytes</title><author>Kim, Jinju ; Park, Hyo-Min ; Lim, Chae-Min ; Jeon, Kyeong-Bae ; Kim, Seonhwa ; Lee, Jin ; Hong, Jin-Tae ; Oh, Deok-Kun ; Yang, Young ; Yoon, Do-Young</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p174t-a179977daabf10dd955ea8954d6d9aae6c1913ef6d50ea52f8c744521f7035233</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Jinju</creatorcontrib><creatorcontrib>Park, Hyo-Min</creatorcontrib><creatorcontrib>Lim, Chae-Min</creatorcontrib><creatorcontrib>Jeon, Kyeong-Bae</creatorcontrib><creatorcontrib>Kim, Seonhwa</creatorcontrib><creatorcontrib>Lee, Jin</creatorcontrib><creatorcontrib>Hong, Jin-Tae</creatorcontrib><creatorcontrib>Oh, Deok-Kun</creatorcontrib><creatorcontrib>Yang, Young</creatorcontrib><creatorcontrib>Yoon, Do-Young</creatorcontrib><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BMB reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Jinju</au><au>Park, Hyo-Min</au><au>Lim, Chae-Min</au><au>Jeon, Kyeong-Bae</au><au>Kim, Seonhwa</au><au>Lee, Jin</au><au>Hong, Jin-Tae</au><au>Oh, Deok-Kun</au><au>Yang, Young</au><au>Yoon, Do-Young</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Specialized pro-resolving mediator 7S MaR1 inhibits IL-6 expression via modulating ROS/p38/ERK/NF-κB pathways in PM10-exposed keratinocytes</atitle><jtitle>BMB reports</jtitle><date>2024-11-01</date><risdate>2024</risdate><volume>57</volume><issue>11</issue><spage>490</spage><epage>496</epage><pages>490-496</pages><issn>1976-670X</issn><issn>1976-6696</issn><eissn>1976-670X</eissn><abstract>Keratinocytes are susceptible to airborne particulate matter (PM) exposure, resulting in human skin barrier dysfunction. Therefore, it is important to find useful reagents to resolve skin damages caused by PM. Here, we explored the protective effect of 7S MaR1, a specialized pro-resolving mediator derived from docosahexaenoic acid, on skin inflammation and the oxidative stress induced by PM with a diameter 10 μm or less (PM10) in human keratinocyte HaCaT cells. Interestingly, PM10-induced ROS generation was modulated by 7S MaR1 via the recovery of ROS scavenger genes. 7S MaR1 reduced PM10-induced IL-6 expression via modulating the p38/ERK/NF-κB signaling pathways. These results demonstrate that PM10 induces inflammatory cytokines, which can lead to skin diseases. In addition, 7S MaR1 can resolve inflammation caused by PM10-induced oxidative stress and inflammatory cytokines. [BMB Reports 2024; 57(11): 490-496].Keratinocytes are susceptible to airborne particulate matter (PM) exposure, resulting in human skin barrier dysfunction. Therefore, it is important to find useful reagents to resolve skin damages caused by PM. Here, we explored the protective effect of 7S MaR1, a specialized pro-resolving mediator derived from docosahexaenoic acid, on skin inflammation and the oxidative stress induced by PM with a diameter 10 μm or less (PM10) in human keratinocyte HaCaT cells. Interestingly, PM10-induced ROS generation was modulated by 7S MaR1 via the recovery of ROS scavenger genes. 7S MaR1 reduced PM10-induced IL-6 expression via modulating the p38/ERK/NF-κB signaling pathways. These results demonstrate that PM10 induces inflammatory cytokines, which can lead to skin diseases. In addition, 7S MaR1 can resolve inflammation caused by PM10-induced oxidative stress and inflammatory cytokines. [BMB Reports 2024; 57(11): 490-496].</abstract><pub>Korean Society for Biochemistry and Molecular Biology</pub><doi>10.5483/BMBRep.2024-0124</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 1976-670X
ispartof BMB reports, 2024-11, Vol.57 (11), p.490-496
issn 1976-670X
1976-6696
1976-670X
language eng
recordid cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_11608853
source PubMed (Medline); Alma/SFX Local Collection; Free Full-Text Journals in Chemistry
title Specialized pro-resolving mediator 7S MaR1 inhibits IL-6 expression via modulating ROS/p38/ERK/NF-κB pathways in PM10-exposed keratinocytes
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-07T19%3A35%3A35IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Specialized%20pro-resolving%20mediator%207S%20MaR1%20inhibits%20IL-6%20expression%20via%20modulating%20ROS/p38/ERK/NF-%CE%BAB%20pathways%20in%20PM10-exposed%20keratinocytes&rft.jtitle=BMB%20reports&rft.au=Kim,%20Jinju&rft.date=2024-11-01&rft.volume=57&rft.issue=11&rft.spage=490&rft.epage=496&rft.pages=490-496&rft.issn=1976-670X&rft.eissn=1976-670X&rft_id=info:doi/10.5483/BMBRep.2024-0124&rft_dat=%3Cproquest_pubme%3E3115095849%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=3115095849&rft_id=info:pmid/&rfr_iscdi=true