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Impact of the Junction Adhesion Molecule-A on Asthma
장안수,안민혁,이푸른하늘,최선묵,황다연,김정현,박명철,박신희,백애린 연세대학교의과대학 2023 Yonsei medical journal Vol.64 No.6
Purpose: Junctional adhesion molecule (JAM)-A is an immunoglobulin-like molecule that colocalizes with tight junctions (TJs) in the endothelium and epithelium. It is also found in blood leukocytes and platelets. The biological significance of JAM-A in asthma, as well as its clinical potential as a therapeutic target, are not well understood. The aim of this study was to elucidate the role of JAM-A in a mouse model of asthma, and to determine blood levels of JAM-A in asthmatic patients. Materials and Methods: Mice sensitized and challenged with ovalbumin (OVA) or saline were used to investigate the role of JAM-A in the pathogenesis of bronchial asthma. In addition, JAM-A levels were measured in the plasma of asthmatic patients and healthy controls. The relationships between JAM-A and clinical variables in patients with asthma were also examined. Results: Plasma JAM-A levels were higher in asthma patients (n=19) than in healthy controls (n=12). In asthma patients, the JAM-A levels correlated with forced expiratory volume in 1 second (FEV1%), FEV1/forced vital capacity (FVC), and the blood lymphocyte proportion. JAM-A, phospho-JNK, and phospho-ERK protein expressions in lung tissue were significantly higher in OVA/OVA mice than in control mice. In human bronchial epithelial cells treated with house dust mite extracts for 4 h, 8 h, and 24 h, the JAM A, phospho-JNK, and phospho-ERK expressions were increased, as shown by Western blotting, while the transepithelial electrical resistance was reduced. Conclusion: These results suggest that JAM-A is involved in the pathogenesis of asthma, and may be a marker for asthma.
Comparison of Protein Profiles in Plasma between Stable and Exacerbation
장안수,( Jeong Seok Heo ),( Jong Sook Park ),( Eun Ju Lee ),( Tae Hoon Kim ),( Sung Woo Park ),( Soo Taek Uh ),( Choon Sik Park ) 대한결핵 및 호흡기학회 2012 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.114 No.-
Background: Cigarette smoking is the major risk factor for several forms of lung disease including COPD. Up to date, no effective therapies to reverse or retard the course of the disease are available. Thus, proteomic analysis of COPD may be important for understanding the pathobiology of COPD at the protein levels. Our study suggested that differentially expressed proteins in human plasma were evaluated for development of COPD. Objective: To identify plasma biomarkers in COPD and to compare protein profiles in plasma between stable and exacerbation with COPD. Methods: We examined the plasma of nomal control (n=8) and COPD stable (n=8) and exacerbation (n=8) using 2-DE, respectively. The differentially expressed protein spots were identified by MALDI-TOF/TOF. ELISA were performed for identification and quantitative measurement of RARα in plasma from nomal control (n=37) and COPD stable (n=35) and exacerbation (n=21). Results: 17 proteins were identified to be differentially expressed in plasma between COPD stable and COPD exacerbation by MALDI-TOF/TOF. We found that 10 proteins were increased in plasma of stable, while 7 proteins were lower in stable than exacerbation. One of these proteins was associated with RARα protein. The result of the subjects with COPD exacerbation had significantly higher plasma levels of RARα than COPD stable and normal control subjects. Conclusion: The proteomic analysis of plasma indicates that alteration of various proteins may be associated with COPD development.