Role of Lung Apolipoprotein A-I in Idiopathic Pulmonary Fibrosis Antiinflammatory and Antifibrotic Effect on Experimental Lung Injury and Fibrosis
- Authors
- Kim, Tae Hoon; Lee, Yoo Hoon; Kim, Kyung Hun; Lee, Shin Hwa; Cha, Ji Yeon; Shin, Eun Kyoung; Jung, Seok; Jang, An Soo; Park, Sung Woo; Uh, Soo Taek; Kim, Young Hoon; Park, Jai Soung; Sin, Hwa Gyoun; Youm, Wook; Koh, Eun Suk; Cho, Sun Young; Paik, Young Ki; Rhim, Tai Youn; Park, Choon Sik
- Issue Date
- Sep-2010
- Publisher
- AMER THORACIC SOC
- Keywords
- fibrosis, pulmonary; idiopathic interstitial pneumonia; apolipoprotein A-I; bleomycin A(2)
- Citation
- AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, v.182, no.5, pp.633 - 642
- Indexed
- SCIE
SCOPUS
- Journal Title
- AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
- Volume
- 182
- Number
- 5
- Start Page
- 633
- End Page
- 642
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/174193
- DOI
- 10.1164/rccm.200905-0659OC
- ISSN
- 1073-449X
- 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.
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