Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 최재훈 | - |
dc.date.accessioned | 2018-03-19T08:18:51Z | - |
dc.date.available | 2018-03-19T08:18:51Z | - |
dc.date.issued | 2014-11 | - |
dc.identifier.citation | PLOS ONE, 권: 9, 호: 11 | en_US |
dc.identifier.issn | 1932-6203 | - |
dc.identifier.uri | http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0112666 | - |
dc.identifier.uri | http://hdl.handle.net/20.500.11754/49081 | - |
dc.description.abstract | Resistin-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.sponsorship | Funding: 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.iso | en | en_US |
dc.publisher | PUBLIC LIBRARY SCIENCE, 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA | en_US |
dc.subject | Animals | en_US |
dc.subject | Asthma | en_US |
dc.subject | genetics | en_US |
dc.subject | metabolism | en_US |
dc.subject | Base Sequence | en_US |
dc.subject | Bronchoalveolar Lavage Fluid | en_US |
dc.subject | DNA Primers | en_US |
dc.subject | Enzyme-Linked Immunosorbent Assay | en_US |
dc.subject | Hypersensitivity | en_US |
dc.title | Retnla Overexpression Attenuates Allergic Inflammation of the Airway | en_US |
dc.type | Article | en_US |
dc.relation.no | 11 | - |
dc.relation.volume | 9 | - |
dc.identifier.doi | 10.1371/journal.pone.0112666 | - |
dc.relation.page | 1-2 | - |
dc.relation.journal | PLOS ONE | - |
dc.contributor.googleauthor | Lee, Mi-Ran | - |
dc.contributor.googleauthor | Shim, Da-hee | - |
dc.contributor.googleauthor | Yoon, Ji-hye | - |
dc.contributor.googleauthor | Jang, Hyung | - |
dc.contributor.googleauthor | Oh, Se-Woong | - |
dc.contributor.googleauthor | Suh, Suk-Hyo | - |
dc.contributor.googleauthor | Choi, Jae-Hoon | - |
dc.contributor.googleauthor | Oh, Goo-Taeg | - |
dc.relation.code | 2014037807 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF NATURAL SCIENCES[S] | - |
dc.sector.department | DEPARTMENT OF LIFE SCIENCE | - |
dc.identifier.pid | jchoi75 | - |
dc.identifier.researcherID | R-6224-2016 | - |
dc.identifier.orcid | http://orcid.org/0000-0002-5265-3463 | - |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.