Role of Lung Apolipoprotein A-I in Idiopathic Pulmonary Fibrosis Antiinflammatory and Antifibrotic Effect on Experimental Lung Injury and Fibrosis
DC Field | Value | Language |
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dc.contributor.author | Kim, Tae Hoon | - |
dc.contributor.author | Lee, Yoo Hoon | - |
dc.contributor.author | Kim, Kyung Hun | - |
dc.contributor.author | Lee, Shin Hwa | - |
dc.contributor.author | Cha, Ji Yeon | - |
dc.contributor.author | Shin, Eun Kyoung | - |
dc.contributor.author | Jung, Seok | - |
dc.contributor.author | Jang, An Soo | - |
dc.contributor.author | Park, Sung Woo | - |
dc.contributor.author | Uh, Soo Taek | - |
dc.contributor.author | Kim, Young Hoon | - |
dc.contributor.author | Park, Jai Soung | - |
dc.contributor.author | Sin, Hwa Gyoun | - |
dc.contributor.author | Youm, Wook | - |
dc.contributor.author | Koh, Eun Suk | - |
dc.contributor.author | Cho, Sun Young | - |
dc.contributor.author | Paik, Young Ki | - |
dc.contributor.author | Rhim, Tai Youn | - |
dc.contributor.author | Park, Choon Sik | - |
dc.date.accessioned | 2022-12-20T15:53:29Z | - |
dc.date.available | 2022-12-20T15:53:29Z | - |
dc.date.created | 2022-08-27 | - |
dc.date.issued | 2010-09 | - |
dc.identifier.issn | 1073-449X | - |
dc.identifier.uri | https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/174193 | - |
dc.description.abstract | Rationale: Idiopathic pulmonary fibrosis (IPF) is caused by alterations in expression of proteins involved in multiple pathways, including matrix deposition, inflammation, injury, and repair. Objectives: To understand the pathogenic changes in lung protein expression in IPF and to evaluate apolipoprotein (Apo) A-I as a candidate therapeutic molecule. Methods: Two-dimensional electrophoresis was adopted for differential display proteomics. Reverse-transcriptase polymerase chain reaction, Western blotting, immunohistochemical staining, and ELISA were performed for identification and quantitative measurement of Apo A-I in bronchoalveolar lavage fluids from subjects with IPF and experimental bleomycin-induced mice. Measurements and Main Results: Sixteen protein spots showed differences in relative intensity between IPF (n = 14) and healthy control subjects (n = 8). Nano liquid chromatography-tandem mass spectrometry (LC-MS/MS) revealed increase of haptoglobulin and decrease of alpha(1)-antitrypsin, alpha(1)-antichymotrypsin, macrophage capping protein, angiotensinogen, hemoglobin chain B, Apo A-I, clusterin, protein disulfide isomerase A3, immunoglobulin, and complement C4A in IPF compared with normal control subjects (P = 0.006-0.044). Apo A-I concentrations were lower in bronchoalveolar lavage fluids from subjects with IPF (n = 28) than in normal control subjects (n = 18; P < 0.01). In bleomycin-treated mice, Apo A-I protein in BALF was lower than that in sham-treated control animals. Immunohistochemical analysis showed positive staining on intraalveolar macrophages and epithelial cells of the lungs. Intranasal treatment with Apo A-I protein reduced the bleomycin-induced increases in number of inflammatory cells and collagen deposition in sham-treated mice in a dose-dependent manner. Conclusions: Alterations of several inflammatory and antiinflammatory proteins in the lungs may be related to the pathogenesis of IPF, and local treatment with Apo A-I is very effective against the development of experimental lung injury and fibrosis. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | AMER THORACIC SOC | - |
dc.title | Role of Lung Apolipoprotein A-I in Idiopathic Pulmonary Fibrosis Antiinflammatory and Antifibrotic Effect on Experimental Lung Injury and Fibrosis | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Rhim, Tai Youn | - |
dc.identifier.doi | 10.1164/rccm.200905-0659OC | - |
dc.identifier.scopusid | 2-s2.0-77957705241 | - |
dc.identifier.wosid | 000281492000008 | - |
dc.identifier.bibliographicCitation | AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, v.182, no.5, pp.633 - 642 | - |
dc.relation.isPartOf | AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE | - |
dc.citation.title | AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE | - |
dc.citation.volume | 182 | - |
dc.citation.number | 5 | - |
dc.citation.startPage | 633 | - |
dc.citation.endPage | 642 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | General & Internal Medicine | - |
dc.relation.journalResearchArea | Respiratory System | - |
dc.relation.journalWebOfScienceCategory | Critical Care Medicine | - |
dc.relation.journalWebOfScienceCategory | Respiratory System | - |
dc.subject.keywordPlus | BRONCHOALVEOLAR LAVAGE FLUID | - |
dc.subject.keywordPlus | INFLAMMATORY RESPONSE | - |
dc.subject.keywordPlus | SYSTEMIC-SCLEROSIS | - |
dc.subject.keywordPlus | MIMETIC PEPTIDE | - |
dc.subject.keywordPlus | APOA-I | - |
dc.subject.keywordPlus | PATHOGENESIS | - |
dc.subject.keywordPlus | SARCOIDOSIS | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | PROTEINS | - |
dc.subject.keywordPlus | PROTEOME | - |
dc.subject.keywordAuthor | fibrosis, pulmonary | - |
dc.subject.keywordAuthor | idiopathic interstitial pneumonia | - |
dc.subject.keywordAuthor | apolipoprotein A-I | - |
dc.subject.keywordAuthor | bleomycin A(2) | - |
dc.identifier.url | https://www.atsjournals.org/doi/10.1164/rccm.200905-0659OC | - |
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