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      KCI등재 SCOPUS SCIE

      Gene Profiles in a Smoke-Induced COPD Mouse Lung Model Following Treatment with Mesenchy-mal Stem Cells

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      https://www.riss.kr/link?id=A103583545

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      다국어 초록 (Multilingual Abstract)

      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 i...

      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.

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      참고문헌 (Reference)

      1 김유선, "Tracking Intravenous Adipose-Derived Mesenchymal Stem Cells in a Model of Elastase-Induced Emphysema" 대한결핵및호흡기학회 77 (77): 116-123, 2014

      2 Aaron, S. D., "Tiotropium in combination with placebo, salmeterol, or fluticasone-salmeterol for treatment of chronic obstructive pulmonary disease : a randomized trial" 146 : 545-555, 2007

      3 Zandi-Nejad, K., "The role of HCA2(GPR109A)in regulating macrophage function" 27 : 4366-4374, 2013

      4 Shapiro, S. D, "The pathogenesis of emphysema : the elastase : antielastase hypothesis 30 years later" 107 : 346-352, 1995

      5 Benarafa, C., "The neutrophil serine protease inhibitor serpinb1 preserves lung defense functions in Pseudomonas aeruginosa infection" 204 : 1901-1909, 2007

      6 Stone, P. J, "The elastase-antielastase hypothesis of the pathogenesis of emphysema" 4 : 405-412, 1983

      7 Calverley, P. M., "Salmeterol and fluticasone propionate and survival in chronic obstructive pulmonary disease" 356 : 775-789, 2007

      8 Hautamaki, R. D., "Requirement for macrophage elastase for cigarette smoke-induced emphysema in mice" 277 : 2002-2004, 1997

      9 Ahmad, M. K., "Protective effect of taurine against potassium bromate-induced hemoglobin oxidation, oxidative stress, and impairment of antioxidant defense system in blood" 31 : 304-313, 2016

      10 Yoshida, T., "Pathobiology of cigarette smoke-induced chronic obstructive pulmonary disease" 87 : 1047-1082, 2007

      1 김유선, "Tracking Intravenous Adipose-Derived Mesenchymal Stem Cells in a Model of Elastase-Induced Emphysema" 대한결핵및호흡기학회 77 (77): 116-123, 2014

      2 Aaron, S. D., "Tiotropium in combination with placebo, salmeterol, or fluticasone-salmeterol for treatment of chronic obstructive pulmonary disease : a randomized trial" 146 : 545-555, 2007

      3 Zandi-Nejad, K., "The role of HCA2(GPR109A)in regulating macrophage function" 27 : 4366-4374, 2013

      4 Shapiro, S. D, "The pathogenesis of emphysema : the elastase : antielastase hypothesis 30 years later" 107 : 346-352, 1995

      5 Benarafa, C., "The neutrophil serine protease inhibitor serpinb1 preserves lung defense functions in Pseudomonas aeruginosa infection" 204 : 1901-1909, 2007

      6 Stone, P. J, "The elastase-antielastase hypothesis of the pathogenesis of emphysema" 4 : 405-412, 1983

      7 Calverley, P. M., "Salmeterol and fluticasone propionate and survival in chronic obstructive pulmonary disease" 356 : 775-789, 2007

      8 Hautamaki, R. D., "Requirement for macrophage elastase for cigarette smoke-induced emphysema in mice" 277 : 2002-2004, 1997

      9 Ahmad, M. K., "Protective effect of taurine against potassium bromate-induced hemoglobin oxidation, oxidative stress, and impairment of antioxidant defense system in blood" 31 : 304-313, 2016

      10 Yoshida, T., "Pathobiology of cigarette smoke-induced chronic obstructive pulmonary disease" 87 : 1047-1082, 2007

      11 Liang, X., "Paracrine mechanisms of mesenchymal stem cell-based therapy : current status and perspectives" 23 : 1045-1059, 2014

      12 Suga, H., "Paracrine mechanism of angiogenesis in adiposederived stem cell transplantation" 72 : 234-241, 2014

      13 Katsha, A. M., "Paracrine factors of multipotent stromal cells ameliorate lung injury in an elastase-induced emphysema model" 19 : 196-203, 2011

      14 MacNee, W., "New paradigms in the pathogenesis of chronic obstructive pulmonary disease I" 6 : 527-531, 2009

      15 Shapiro, S. D., "Neutrophil elastase contributes to cigarette smoke-induced emphysema in mice" 163 : 2329-2335, 2003

      16 Matthew B Murphy, "Mesenchymal stem cells: environmentally responsive therapeutics for regenerative medicine" 생화학분자생물학회 45 : 1-16, 2013

      17 Lee, R. H., "Intravenous hMSCs improve myocardial infarction in mice because cells embolized in lung are activated to secrete the anti-inflammatory protein TSG-6" 5 : 54-63, 2009

      18 Yang, J. Y., "Integration microarray and regulation datasets for chronic obstructive pulmonary disease" 17 : 1923-1931, 2013

      19 Halappanavar, S., "Induction of the interleukin 6/ signal transducer and activator of transcription pathway in the lungs of mice sub-chronically exposed to mainstream tobacco smoke" 2 : 56-, 2009

      20 Macari, E. R., "Induction of human fetal hemoglobin via the NRF2 antioxidant response signaling pathway" 117 : 5987-5997, 2011

      21 Chen, Z. H., "Identifying targets for COPD treatment through gene expression analyses" 3 : 359-370, 2008

      22 Grek, C. L., "Hypoxia up-regulates expression of hemoglobin in alveolar epithelial cells" 44 : 439-447, 2011

      23 Henning, R. J., "Human cord blood stem cell paracrine factors activate the survival protein kinase Akt and inhibit death protein kinases JNK and p38 in injured cardiomyocytes" 16 : 1158-1168, 2014

      24 Huffman, L. J., "Hemoglobin potentiates the production of reactive oxygen species by alveolar macrophages" 26 : 203-217, 2000

      25 Newton, D. A., "Hemoglobin is expressed by alveolar epithelial cells" 281 : 5668-5676, 2006

      26 Rabe, K. F., "Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease : GOLD executive summary" 176 : 532-555, 2007

      27 Banks, M. F., "Egr-1 antisense oligonucleotides inhibit hypoxia-induced proliferation of pulmonary artery adventitial fibroblasts" 98 (98): 732-738, 2005

      28 Rangasamy, T., "Cigarette smoke-induced emphysema in A/J mice is associated with pulmonary oxidative stress, apoptosis of lung cells, and global alterations in gene expression" 296 : 888-900, 2009

      29 Huh, J. W., "Bone marrow cells repair cigarette smoke-induced emphysema in rats" 301 : 255-266, 2011

      30 Schweitzer, K. S., "Adipose stem cell treatment in mice attenuates lung and systemic injury induced by cigarette smoking" 183 : 215-225, 2011

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      2023 평가예정 해외DB학술지평가 신청대상 (해외등재 학술지 평가)
      2020-01-01 평가 등재학술지 유지 (해외등재 학술지 평가) KCI등재
      2012-11-07 학술지명변경 한글명 : 분자와 세포 -> Molecules and Cells KCI등재
      2008-01-01 평가 SCI 등재 (등재유지) KCI등재
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      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
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      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
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