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Inhibition of Vitamin D Receptor Translocation by Cigarette Smoking Extracts
어수택,박춘식,So-My Koo,김양기,장안수,김도진,김용훈,박성우,김기업 대한결핵및호흡기학회 2012 Tuberculosis and Respiratory Diseases Vol.73 No.5
Background: Vitamin D can translocate a vitamin D receptor (VDR) from the nucleus to the cell membranes. The meaning of this translocation is not elucidated in terms of a role in pathogenesis of chronic obstructive pulmonary disease (COPD) till now. VDR deficient mice are prone to develop emphysema, suggesting that abnormal function of VDR might influence a generation of COPD. The blood levels of vitamin D have known to be well correlated with that of lung function in patients with COPD, and smoking is the most important risk factor in development of COPD. This study was performed to investigate whether cigarette smoke extracts (CSE) can inhibit the translocation of VDR and whether mitogen activated protein kinases (MAPKs) are involved in this inhibition. Methods: Human alveolar basal epithelial cell line (A549) was used in this study. 1,25-(OH2)D3 and/or MAPKs inhibitors and antioxidants were pre-incubated before stimulation with 10% CSE, and then nucleus and microsomal proteins were extracted for a Western blot of VDR. Results: Five minutes treatment of 1,25-(OH2)D3 induced translocation of VDR from nucleus to microsomes by a dose-dependent manner. CSE inhibited 1,25-(OH2)D3-induced translocation of VDR in both concentrations of 10% and 20%. All MAPKs inhibitors did not suppress the inhibitory effects of CSE on the 1,25-(OH2)D3-induced translocation of VDR. Quercetin suppressed the inhibitory effects of CSE on the 1,25-(OH2)D3-induced translocation of VDR, but not in n-acetylcysteine. Conclusion: CSE has an ability to inhibit vitamin D-induced VDR translocation, but MAPKs are not involved in this inhibition.
어수택,Choon Sik Park,Ji Yeon Lee,So Mi Koo,김양기,Ki Up Kim,박종숙,박성우,장안수,김도진,Jae Sung Choi,나주옥,서기현,Yong Hoon Kim 대한결핵및호흡기학회 2011 Tuberculosis and Respiratory Diseases Vol.70 No.6
Background: Chronic obstructive pulmonary disease (COPD) is characterized by air flow limitation, which is one of the leading causes of mortality worldwide. There have been many studies on survival rates in the world literature, but there have been few reports regarding the survival rate in Korean patients with COPD. Acute exacerbation is regarded as a risk factor for mortality in patients with COPD. The purpose of this study was to investigate the survival rate and the effect of acute exacerbations on the survival rate of Korean patients with COPD. Methods: A total of 502 COPD patients who were diagnosed on the basis of history and lung function tests were enrolled in this study. The frequency of acute exacerbations, body mass index (BMI), C-reactive protein (CRP) and pulmonary hypertension were analyzed. Results: The 3- and 5-year survival rates were 98% and 83%, respectively. The median survival time was 78 months. The median survival time was 55 months in 322 patients with one or more acute exacerbations. The 3- and 5-year survival rates were significantly lower in the 322 patients with one or more acute exacerbations than in those without any. The mortality rate was significantly higher in patients with CRP >3 mg/L than in those with CRP ≤3 mg/L (p<0.005); it was significantly higher in patients with pulmonary hypertension than in those without it (p<0.01). Conclusion: Because the 5-year survival rate is 83% in Korean patients with COPD, the management of stable patients with COPD should focus on the prevention of acute exacerbations.
유리규산에 의한 대식세포의 활성화 과정에서 최염성 cytokine의 역할
어수택,이중달 한양대학교 의과대학 1999 한양의대 학술지 Vol.19 No.1
Chronic inhalation of silica induces lung fibrosis. The alveolar macrophages ingest the inhaled silica and they liberate the various cytokines which evoke pulmonary fibrosis. However, the pathogensis of pulmonary fibrosis induced by silica inhalation has not been defined yet. This study has undertaken to evaluate pathogenesis of silica-induced pulmonary fibrosis by measurement of proinflammatory cytokines. Mouse macrophage cell line, RAW 264.7, was used in this study. Macrophages were stimulated by silica(SiO_2) in the various concentrations for 2, 4, 8, 12, 24, and 48 hours. The supernatants were used for the measurement of protein levels by bioassay, and cells for the levels of mRNA by Northern blot and in situ hybridization. Followings are results obtained. 1) The production of IL-6 was not observed untill 4 hours, and reached the peak levels at 12 hours after stimulation of silica. The production of TNF-α increased from 4 hours and reached the peak levels at 24 hours after stimulation of silica. The spontaneous TGF-β production reached the peak levels at 24 hours. 2) The blots of IL-6 were observed from 8 hours and not observed at 48 hours after stimulation of silica. The blots of TNF-α appeared from 4 hours and reached the peak levels at 24 hours after stimulation of silica. In contrast, the blot of TGF-β was observed at two hours and the density of blots decreased at 24 and 48 hours after stimulation of silica. 3) In situ hybridization revealed the increased positive signals at eight hours in IL-6, at 4 hours in TNF-α, and 8 hours in TGF-β. The results above suggest that TNF-α and IL-6 liberated from macrophages activated by silica may induce fibrosis, and that TNF-α and TGF-β play a different role in fibrosis.
어수택 대한의사협회 2009 대한의사협회지 Vol.52 No.1
Idiopathic pulmonary fibrosis (IPF) is characterized by chronic progressive parenchymal lung fibrosis. Although extensive researches for IPF pathogenesis have been reported for several decades, the precise mechanisms are still unknown and the specific treatments for elimination of fibrosis and prolongation of survival are also still unknown. The role of inflammation as initial insult of lung fibrosis is still debating by controversial results of animal model experiments. The recent proposed mechanism for IPF is a dysregulation of epithelial-mesenchymal interactions which have critical role in tissue repair process and fibrosis. This hypothesis suggests impaired communications between epithelium and mesenchymal cells in terms of abnormal proliferation of mesenchymal cells instead of normal proliferation of epithelium. At recent, epithelial mesenchymal transition is regarded as an important source of myofiborblast which are major cells producing extracellular matrix. Classical treatment agents including steroid are already known to be ineffective in treatment of IPF, and also, IFN- one of newly emerging drug, is proved to be ineffective in treatment of IPF. Now new drugs involved in the molecular levels of signal transduction of fibrotic pathway, inhibition of various growth factors (TGF, CTGF, VEGF), and direct inhibition of fibrotic cytokines are under investigated in animal experiments and human clinical studies. Further studies should be focused on the evaluation of precipitating factors, genetic markers, drugs for inhibiting specific molecules responsible for lung fibrosis, and agents for controlling ECM precipitation.
어수택,김양기,이영목 순천향의학연구소 2004 Journal of Soonchunhyang Medical Science Vol.10 No.2
A bronchial carcinoid tumor is identified in the patients with cough and normal chest PA or during routine examination of chest PA. Sometimes it is very difficult to diagnose the bronchial carcinoid tumor with normal chest PA, especially if the patient complains the typical symptoms of bronchial asthma. We experienced a 30 year-old female, who had been suffered from coughing and dyspnea in spite of asthma medications for 1 year, with bronchial carcinoid tumor. We describe here a case of bronchial carcinoid tumor mimicking refractory bronchial asthma.