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Kim, You-Sun,Hong, Goohyeon,Kim, Doh Hyung,Kim, Young Min,Kim, Yoon-Keun,Oh, Yeon-Mok,Jee, Young-Koo Nature Publishing Group UK 2018 Experimental and molecular medicine Vol.50 No.11
<▼1><P>Although the positive effects of recombinant fibroblast growth factor-2 (rFGF-2) in chronic obstructive pulmonary disease (COPD) have been implicated in previous studies, knowledge of its role in COPD remains limited. The mechanism of FGF2 in a COPD mouse model and the therapeutic potential of rFGF-2 were investigated in COPD. The mechanism and protective effects of rFGF-2 were evaluated in cigarette smoke-exposed or elastase-induced COPD animal models. Inflammation was assessed in alveolar cells and lung tissues from mice. FGF-2 was decreased in the lungs of cigarette smoke-exposed mice. Intranasal use of rFGF-2 significantly reduced macrophage-dominant inflammation and alveolar destruction in the lungs. In the elastase-induced emphysema model, rFGF-2 improved regeneration of the lungs. In humans, plasma FGF-2 was decreased significantly in COPD compared with normal subjects (10 subjects, <I>P</I> <I>=</I> 0.037). The safety and efficacy of inhaled rFGF-2 use was examined in COPD patients, along with changes in respiratory symptoms and pulmonary function. A 2-week treatment with inhaled rFGF-2 in COPD (<I>n</I> = 6) resulted in significantly improved respiratory symptoms compared with baseline levels (<I>P</I> <I><</I> 0.05); however, the results were not significant compared with the placebo. The pulmonary function test results of COPD improved numerically compared with those in the placebo, but the difference was not statistically significant. No serious adverse events occurred during treatment with inhaled rFGF-2. The loss of FGF-2 production is an important mechanism in the development of COPD. Inhaling rFGF-2 may be a new therapeutic option for patients with COPD because rFGF-2 decreases inflammation in lungs exposed to cigarette smoke.</P></▼1><▼2><P><B>Lung disease: Inhaling a protein might help</B></P><P>Studies on the role of the protein ‘fibroblast growth factor-2’ (FGF-2) in chronic obstructive pulmonary disease (COPD) suggest that inhaled FGF-2 could help treat the emphysema linked to smoking. Researchers in South Korea led by Young-Koo Jee at Dankook University, Cheonan, and Yeon-Mok Oh at the University of Ulsan, Seoul, studied the role of the reduced FGF-2 levels found in mice with lung inflammation caused by exposure to cigarette smoke. They also uncovered details of a protective effect of inhaled FGF-2, identifying specific cellular and lung structure changes attributed to the administered FGF-2. Reduced FGF-2 levels were also found in patients with COPD. Initial trials revealed some improvement in patients treated with FGF-2, but not at a statistically significant level. Nevertheless, the authors suggest their results justify further investigation of the protein’s therapeutic potential.</P></▼2>
Yeon-Mok Oh,You-Sun Kim,Nurdan Kokturk,Ji-Young Kim,Sei Won Lee,Jaeyun Lim,Soo Jin Choi,Wonil Oh 한국분자세포생물학회 2016 Molecules and cells Vol.39 No.10
Mesenchymal stem cells (MSCs) effectively reduce airway inflammation and regenerate the alveolus in cigarette- and elastase-induced chronic obstructive pulmonary disease (COPD) animal models. The effects of stem cells are thought to be paracrine and immune-modulatory because very few stem cells remain in the lung one day after their systemic injection, which has been demonstrated previously. In this report, we analyzed the gene expression profiles to compare mouse lungs with chronic exposure to cigarette smoke with non-exposed lungs. Gene expression profiling was also conducted in a mouse lung tissue with chronic exposure to cigarette smoke following the systemic injection of human cord blood-derived mesenchymal stem cells (hCB-MSCs). Globally, 834 genes were differentially expressed after systemic injection of hCB-MSCs. Seven and 21 genes, respectively, were up-and down-regulated on days 1, 4, and 14 after HCB-MSC injection. The Hbb and Hba, genes with oxygen transport and anti-oxidant functions, were increased on days 1 and 14. A serine protease inhibitor was also increased at a similar time point after injection of hCB-MSCs. Gene Ontology analysis indicated that the levels of genes related to immune responses, metabolic processes, and blood vessel development were altered, indicating host responses after hCB-MSC injection. These gene expression changes suggest that MSCs induce a regeneration mechanism against COPD induced by cigarette smoke. These analyses provide basic data for understanding the regeneration mechanisms promoted by hCB-MSCs in cigarette smoke-induced COPD.
Retroviral Vector를 이용한 TNF-α 유전자의 이입이 암세포의 종양괴사인자(TNF) 감수성에 미치는 효과
오연목 ( Yeon Mok Oh ),박계영 ( Kyeo Yeong Park ),정만표 ( Man Pyo Jung ),유철규 ( Chul Gyu Yoo ),김영환 ( Young Whan Kim ),한성구 ( Sung Goo Han ),심영수 ( Young Soo Sim ),한용철 ( Yong Chol Han ) 대한결핵 및 호흡기학회 1994 Tuberculosis and Respiratory Diseases Vol.41 No.2
만성폐쇄성폐질환과 천식을 감별 진단하는데 기관지확장제 가역성 검사의 역할
오연목 ( Yeon Mok Oh ),임채만 ( Chae Man Lim ),심태선 ( Tae Sun Shim ),고윤석 ( Youn Suck Koh ),김우성 ( Woo Sung Kim ),김동순 ( Dong Soon Kim ),김원동 ( Won Dong Kim ),김세규 ( Se Kyu Kim ),유지홍 ( Jee Hong Yoo ),이상도 ( Sang D 대한결핵 및 호흡기학회 2004 Tuberculosis and Respiratory Diseases Vol.57 No.5