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dc.contributor.author최재훈-
dc.date.accessioned2018-03-19T08:18:51Z-
dc.date.available2018-03-19T08:18:51Z-
dc.date.issued2014-11-
dc.identifier.citationPLOS ONE, 권: 9, 호: 11en_US
dc.identifier.issn1932-6203-
dc.identifier.urihttp://journals.plos.org/plosone/article?id=10.1371/journal.pone.0112666-
dc.identifier.urihttp://hdl.handle.net/20.500.11754/49081-
dc.description.abstractResistin-like molecule alpha (Retnla), also known as ` Found in inflammatory zone 1', is a secreted protein that has been found in bronchoalveolar lavage (BAL) fluid of ovalbumin (OVA)-induced asthmatic mice and plays a role as a regulator of T helper (Th) 2-driven inflammation. However, the role of Retnla in the progress of Th2-driven airway inflammation is not yet clear. To better understand the function of Retnla in Th2driven airway inflammation, we generated Retnla-overexpressing (Retnla-Tg) mice. Retnla-Tg mice showed increased expression of Retnla protein in BAL fluid and airway epithelial cells. Retnla overexpression itself did not induce any alteration in lung histology or lung function compared to non-Tg controls. However, OVA-sensitized/ challenged Retnla-Tg mice had decreased numbers of cells in BAL and inflammatory cells accumulating in the lung. They also showed a reduction in mucus production in the airway epithelium, concomitant with a decreased Muc5ac level. These results were accompanied by reduced levels of Th2 cytokines, including interleukin (IL)-4, IL5, and IL-13, with no effect on levels of OVA-specific immunoglobulin isotypes. Furthermore, phosphorylation of ERK was markedly reduced in the lungs of OVAchallenged Retnla-Tg mice. Taken together, these results indicates that Retnla protects against Th2-mediated inflammation in an experimental mouse model of asthma, suggesting that therapeutic approaches to enhance the production of Retnla or Retnla-like molecules could be valuable for preventing allergic lung inflammation.en_US
dc.description.sponsorshipFunding: This work was supported by National Research Foundation of Korea (NRF) grants funded by the Korean government (MEST) (No. 2012R1A3A2026454 (GTO), No. 2010-0019866 (GTO), No. 2013R1A1A1063441 (JHC), No. 2013S1A2A2035348 (JHC), and the research fund of Hanyang University (HY-2012-N)(JHC). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.en_US
dc.language.isoenen_US
dc.publisherPUBLIC LIBRARY SCIENCE, 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USAen_US
dc.subjectAnimalsen_US
dc.subjectAsthmaen_US
dc.subjectgeneticsen_US
dc.subjectmetabolismen_US
dc.subjectBase Sequenceen_US
dc.subjectBronchoalveolar Lavage Fluiden_US
dc.subjectDNA Primersen_US
dc.subjectEnzyme-Linked Immunosorbent Assayen_US
dc.subjectHypersensitivityen_US
dc.titleRetnla Overexpression Attenuates Allergic Inflammation of the Airwayen_US
dc.typeArticleen_US
dc.relation.no11-
dc.relation.volume9-
dc.identifier.doi10.1371/journal.pone.0112666-
dc.relation.page1-2-
dc.relation.journalPLOS ONE-
dc.contributor.googleauthorLee, Mi-Ran-
dc.contributor.googleauthorShim, Da-hee-
dc.contributor.googleauthorYoon, Ji-hye-
dc.contributor.googleauthorJang, Hyung-
dc.contributor.googleauthorOh, Se-Woong-
dc.contributor.googleauthorSuh, Suk-Hyo-
dc.contributor.googleauthorChoi, Jae-Hoon-
dc.contributor.googleauthorOh, Goo-Taeg-
dc.relation.code2014037807-
dc.sector.campusS-
dc.sector.daehakCOLLEGE OF NATURAL SCIENCES[S]-
dc.sector.departmentDEPARTMENT OF LIFE SCIENCE-
dc.identifier.pidjchoi75-
dc.identifier.researcherIDR-6224-2016-
dc.identifier.orcidhttp://orcid.org/0000-0002-5265-3463-
Appears in Collections:
COLLEGE OF NATURAL SCIENCES[S](자연과학대학) > LIFE SCIENCE(생명과학과) > Articles
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