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Kawasaki disease OX40–OX40L axis acts as an upstream regulator of NFAT signaling pathway
Background We investigated a costimulatory molecule OX40–OX40L acting as an upstream regulator to regulate the nuclear factor of activated T cell (NFAT) in the acute phase of Kawasaki disease (KD). Methods One hundred and one samples were collected and divided into six groups: coronary artery lesion...
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Published in: | Pediatric research 2019-05, Vol.85 (6), p.835-840 |
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container_title | Pediatric research |
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creator | Lv, Yu-Wen Chen, Ye Lv, Hai-Tao Li, Xuan Tang, Yun-Jia Qian, Wei-Guo Xu, Qiu-Qin Sun, Ling Qian, Guang-Hui Ding, Yue-Yue |
description | Background
We investigated a costimulatory molecule OX40–OX40L acting as an upstream regulator to regulate the nuclear factor of activated T cell (NFAT) in the acute phase of Kawasaki disease (KD).
Methods
One hundred and one samples were collected and divided into six groups: coronary artery lesion (KD-CAL) before intravenous immunoglobulin (IVIG), KD-CAL after IVIG, KD without CAL (KD-nCAL) before IVIG, KD-nCAL after IVIG, fever of unknown (Fou), and Healthy. In vitro OX40-stimulating and OX40L-inhibiting tests were conducted in Healthy and KD groups, respectively. Both the messenger RNA (mRNA) and protein expression levels of OX40, OX40L, NFAT1, and NFAT2 were investigated using quantitative reverse transcription PCR and immunoblotting assay, respectively.
Results
The mRNA and protein expression levels of NFAT1, NFAT2, OX40, and OX40L were significantly increased in KD-CAL and KD-nCAL groups before IVIG compared with Fou and Healthy groups and decreased after IVIG. A positive correlation was found between them in KD. In vitro OX40-stimulating test demonstrated the significantly increased mRNA and protein expression levels of NFAT1 and NFAT2 in the peripheral blood mononuclear cells of the Healthy group. Meanwhile, OX40L-inhibiting test showed significantly decreased expression levels of NFAT1 and NFAT2 in the KD group.
Conclusion
OX40–OX40L acts as an upstream regulator in the NFAT signaling pathway involved in KD. |
doi_str_mv | 10.1038/s41390-019-0312-0 |
format | article |
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We investigated a costimulatory molecule OX40–OX40L acting as an upstream regulator to regulate the nuclear factor of activated T cell (NFAT) in the acute phase of Kawasaki disease (KD).
Methods
One hundred and one samples were collected and divided into six groups: coronary artery lesion (KD-CAL) before intravenous immunoglobulin (IVIG), KD-CAL after IVIG, KD without CAL (KD-nCAL) before IVIG, KD-nCAL after IVIG, fever of unknown (Fou), and Healthy. In vitro OX40-stimulating and OX40L-inhibiting tests were conducted in Healthy and KD groups, respectively. Both the messenger RNA (mRNA) and protein expression levels of OX40, OX40L, NFAT1, and NFAT2 were investigated using quantitative reverse transcription PCR and immunoblotting assay, respectively.
Results
The mRNA and protein expression levels of NFAT1, NFAT2, OX40, and OX40L were significantly increased in KD-CAL and KD-nCAL groups before IVIG compared with Fou and Healthy groups and decreased after IVIG. A positive correlation was found between them in KD. In vitro OX40-stimulating test demonstrated the significantly increased mRNA and protein expression levels of NFAT1 and NFAT2 in the peripheral blood mononuclear cells of the Healthy group. Meanwhile, OX40L-inhibiting test showed significantly decreased expression levels of NFAT1 and NFAT2 in the KD group.
Conclusion
OX40–OX40L acts as an upstream regulator in the NFAT signaling pathway involved in KD.</description><identifier>ISSN: 0031-3998</identifier><identifier>EISSN: 1530-0447</identifier><identifier>DOI: 10.1038/s41390-019-0312-0</identifier><identifier>PMID: 30723312</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>Case-Control Studies ; Child, Preschool ; Clinical Research Article ; Female ; Humans ; Immunoglobulins, Intravenous - therapeutic use ; Infant ; Kawasaki disease ; Kinases ; Leukocytes, Mononuclear - immunology ; Male ; Medicine ; Medicine & Public Health ; Mucocutaneous Lymph Node Syndrome - genetics ; Mucocutaneous Lymph Node Syndrome - immunology ; Mucocutaneous Lymph Node Syndrome - therapy ; NFATC Transcription Factors - blood ; NFATC Transcription Factors - genetics ; OX40 Ligand - blood ; OX40 Ligand - genetics ; Pediatric Surgery ; Pediatrics ; Protein expression ; Proteins ; Receptors, OX40 - blood ; Receptors, OX40 - genetics ; RNA, Messenger - blood ; RNA, Messenger - genetics ; Signal Transduction</subject><ispartof>Pediatric research, 2019-05, Vol.85 (6), p.835-840</ispartof><rights>International Pediatric Research Foundation, Inc 2019</rights><rights>2019© International Pediatric Research Foundation, Inc 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c415t-dda151cdab0ebacf60ac0152858ea3a076a61a218a9e68a8cda44bc7081422773</citedby><cites>FETCH-LOGICAL-c415t-dda151cdab0ebacf60ac0152858ea3a076a61a218a9e68a8cda44bc7081422773</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30723312$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lv, Yu-Wen</creatorcontrib><creatorcontrib>Chen, Ye</creatorcontrib><creatorcontrib>Lv, Hai-Tao</creatorcontrib><creatorcontrib>Li, Xuan</creatorcontrib><creatorcontrib>Tang, Yun-Jia</creatorcontrib><creatorcontrib>Qian, Wei-Guo</creatorcontrib><creatorcontrib>Xu, Qiu-Qin</creatorcontrib><creatorcontrib>Sun, Ling</creatorcontrib><creatorcontrib>Qian, Guang-Hui</creatorcontrib><creatorcontrib>Ding, Yue-Yue</creatorcontrib><title>Kawasaki disease OX40–OX40L axis acts as an upstream regulator of NFAT signaling pathway</title><title>Pediatric research</title><addtitle>Pediatr Res</addtitle><addtitle>Pediatr Res</addtitle><description>Background
We investigated a costimulatory molecule OX40–OX40L acting as an upstream regulator to regulate the nuclear factor of activated T cell (NFAT) in the acute phase of Kawasaki disease (KD).
Methods
One hundred and one samples were collected and divided into six groups: coronary artery lesion (KD-CAL) before intravenous immunoglobulin (IVIG), KD-CAL after IVIG, KD without CAL (KD-nCAL) before IVIG, KD-nCAL after IVIG, fever of unknown (Fou), and Healthy. In vitro OX40-stimulating and OX40L-inhibiting tests were conducted in Healthy and KD groups, respectively. Both the messenger RNA (mRNA) and protein expression levels of OX40, OX40L, NFAT1, and NFAT2 were investigated using quantitative reverse transcription PCR and immunoblotting assay, respectively.
Results
The mRNA and protein expression levels of NFAT1, NFAT2, OX40, and OX40L were significantly increased in KD-CAL and KD-nCAL groups before IVIG compared with Fou and Healthy groups and decreased after IVIG. A positive correlation was found between them in KD. In vitro OX40-stimulating test demonstrated the significantly increased mRNA and protein expression levels of NFAT1 and NFAT2 in the peripheral blood mononuclear cells of the Healthy group. Meanwhile, OX40L-inhibiting test showed significantly decreased expression levels of NFAT1 and NFAT2 in the KD group.
Conclusion
OX40–OX40L acts as an upstream regulator in the NFAT signaling pathway involved in KD.</description><subject>Case-Control Studies</subject><subject>Child, Preschool</subject><subject>Clinical Research Article</subject><subject>Female</subject><subject>Humans</subject><subject>Immunoglobulins, Intravenous - therapeutic use</subject><subject>Infant</subject><subject>Kawasaki disease</subject><subject>Kinases</subject><subject>Leukocytes, Mononuclear - immunology</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mucocutaneous Lymph Node Syndrome - genetics</subject><subject>Mucocutaneous Lymph Node Syndrome - immunology</subject><subject>Mucocutaneous Lymph Node Syndrome - therapy</subject><subject>NFATC Transcription Factors - blood</subject><subject>NFATC Transcription Factors - genetics</subject><subject>OX40 Ligand - blood</subject><subject>OX40 Ligand - genetics</subject><subject>Pediatric Surgery</subject><subject>Pediatrics</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Receptors, OX40 - blood</subject><subject>Receptors, OX40 - genetics</subject><subject>RNA, Messenger - blood</subject><subject>RNA, Messenger - genetics</subject><subject>Signal Transduction</subject><issn>0031-3998</issn><issn>1530-0447</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNp1kM9Kw0AQxhdRbK0-gBdZ8OIlOrO7STZHEf9hsZcK4iVMk21NTZO6m6C9-Q6-oU_i1lYFQRhmYOb3fbt8jO0jHCNIfeIUygQCwCQAiSKADdbFUPqNUvEm64LfBjJJdIftODcFQBVqtc06EmIhvaLLHm7ohRw9FTwvnCFn-OBewcfb-3L0Ob0WjlPW-Oar4u3cNdbQjFszaUtqasvrMb-9OB1yV0wqKotqwufUPL7QYpdtjal0Zm89e-zu4nx4dhX0B5fXZ6f9IFMYNkGeE4aY5TQCM6JsHAFlgKHQoTYkCeKIIiSBmhITadKeVGqUxaBRCRHHsseOVr5zWz-3xjXprHCZKUuqTN26VHitRBDREj38g07r1vpvf1GxiiAMhadwRWW2ds6acTq3xYzsIkVIl8Gnq-BTH3y6DN63HjtYO7ejmcl_FN9Je0CsAOdP1cTY36f_d_0EOVWMqA</recordid><startdate>20190501</startdate><enddate>20190501</enddate><creator>Lv, Yu-Wen</creator><creator>Chen, Ye</creator><creator>Lv, Hai-Tao</creator><creator>Li, Xuan</creator><creator>Tang, Yun-Jia</creator><creator>Qian, Wei-Guo</creator><creator>Xu, Qiu-Qin</creator><creator>Sun, Ling</creator><creator>Qian, Guang-Hui</creator><creator>Ding, Yue-Yue</creator><general>Nature Publishing Group US</general><general>Nature Publishing Group</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20190501</creationdate><title>Kawasaki disease OX40–OX40L axis acts as an upstream regulator of NFAT signaling pathway</title><author>Lv, Yu-Wen ; Chen, Ye ; Lv, Hai-Tao ; Li, Xuan ; Tang, Yun-Jia ; Qian, Wei-Guo ; Xu, Qiu-Qin ; Sun, Ling ; Qian, Guang-Hui ; Ding, Yue-Yue</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c415t-dda151cdab0ebacf60ac0152858ea3a076a61a218a9e68a8cda44bc7081422773</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Case-Control Studies</topic><topic>Child, Preschool</topic><topic>Clinical Research Article</topic><topic>Female</topic><topic>Humans</topic><topic>Immunoglobulins, Intravenous - therapeutic use</topic><topic>Infant</topic><topic>Kawasaki disease</topic><topic>Kinases</topic><topic>Leukocytes, Mononuclear - immunology</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mucocutaneous Lymph Node Syndrome - genetics</topic><topic>Mucocutaneous Lymph Node Syndrome - immunology</topic><topic>Mucocutaneous Lymph Node Syndrome - therapy</topic><topic>NFATC Transcription Factors - blood</topic><topic>NFATC Transcription Factors - genetics</topic><topic>OX40 Ligand - blood</topic><topic>OX40 Ligand - genetics</topic><topic>Pediatric Surgery</topic><topic>Pediatrics</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Receptors, OX40 - blood</topic><topic>Receptors, OX40 - genetics</topic><topic>RNA, Messenger - blood</topic><topic>RNA, Messenger - genetics</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lv, Yu-Wen</creatorcontrib><creatorcontrib>Chen, Ye</creatorcontrib><creatorcontrib>Lv, Hai-Tao</creatorcontrib><creatorcontrib>Li, Xuan</creatorcontrib><creatorcontrib>Tang, Yun-Jia</creatorcontrib><creatorcontrib>Qian, Wei-Guo</creatorcontrib><creatorcontrib>Xu, Qiu-Qin</creatorcontrib><creatorcontrib>Sun, Ling</creatorcontrib><creatorcontrib>Qian, Guang-Hui</creatorcontrib><creatorcontrib>Ding, Yue-Yue</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Pediatric research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lv, Yu-Wen</au><au>Chen, Ye</au><au>Lv, Hai-Tao</au><au>Li, Xuan</au><au>Tang, Yun-Jia</au><au>Qian, Wei-Guo</au><au>Xu, Qiu-Qin</au><au>Sun, Ling</au><au>Qian, Guang-Hui</au><au>Ding, Yue-Yue</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Kawasaki disease OX40–OX40L axis acts as an upstream regulator of NFAT signaling pathway</atitle><jtitle>Pediatric research</jtitle><stitle>Pediatr Res</stitle><addtitle>Pediatr Res</addtitle><date>2019-05-01</date><risdate>2019</risdate><volume>85</volume><issue>6</issue><spage>835</spage><epage>840</epage><pages>835-840</pages><issn>0031-3998</issn><eissn>1530-0447</eissn><abstract>Background
We investigated a costimulatory molecule OX40–OX40L acting as an upstream regulator to regulate the nuclear factor of activated T cell (NFAT) in the acute phase of Kawasaki disease (KD).
Methods
One hundred and one samples were collected and divided into six groups: coronary artery lesion (KD-CAL) before intravenous immunoglobulin (IVIG), KD-CAL after IVIG, KD without CAL (KD-nCAL) before IVIG, KD-nCAL after IVIG, fever of unknown (Fou), and Healthy. In vitro OX40-stimulating and OX40L-inhibiting tests were conducted in Healthy and KD groups, respectively. Both the messenger RNA (mRNA) and protein expression levels of OX40, OX40L, NFAT1, and NFAT2 were investigated using quantitative reverse transcription PCR and immunoblotting assay, respectively.
Results
The mRNA and protein expression levels of NFAT1, NFAT2, OX40, and OX40L were significantly increased in KD-CAL and KD-nCAL groups before IVIG compared with Fou and Healthy groups and decreased after IVIG. A positive correlation was found between them in KD. In vitro OX40-stimulating test demonstrated the significantly increased mRNA and protein expression levels of NFAT1 and NFAT2 in the peripheral blood mononuclear cells of the Healthy group. Meanwhile, OX40L-inhibiting test showed significantly decreased expression levels of NFAT1 and NFAT2 in the KD group.
Conclusion
OX40–OX40L acts as an upstream regulator in the NFAT signaling pathway involved in KD.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>30723312</pmid><doi>10.1038/s41390-019-0312-0</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Case-Control Studies Child, Preschool Clinical Research Article Female Humans Immunoglobulins, Intravenous - therapeutic use Infant Kawasaki disease Kinases Leukocytes, Mononuclear - immunology Male Medicine Medicine & Public Health Mucocutaneous Lymph Node Syndrome - genetics Mucocutaneous Lymph Node Syndrome - immunology Mucocutaneous Lymph Node Syndrome - therapy NFATC Transcription Factors - blood NFATC Transcription Factors - genetics OX40 Ligand - blood OX40 Ligand - genetics Pediatric Surgery Pediatrics Protein expression Proteins Receptors, OX40 - blood Receptors, OX40 - genetics RNA, Messenger - blood RNA, Messenger - genetics Signal Transduction |
title | Kawasaki disease OX40–OX40L axis acts as an upstream regulator of NFAT signaling pathway |
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