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      Macrophage Depletion by Clodronate Liposomes Suppresses Neointimal Formation After Carotid Artery Injury in Apolipoprotein E-Deficient Mice

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      https://www.riss.kr/link?id=A104687219

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      다국어 초록 (Multilingual Abstract)

      Background and Objectives : Clodronate liposomes deplete phagocytic cels, thereby suppresing inflammation after vascular injury. We compared the efect of clodronate liposomes on macrophage depletion and neointimal formation in apolipoprotein E-deficie...

      Background and Objectives : Clodronate liposomes deplete phagocytic cels, thereby suppresing inflammation after vascular injury. We compared the efect of clodronate liposomes on macrophage depletion and neointimal formation in apolipoprotein E-deficient mice [ApoE (-) mice]. Materials and Methods : ApoE (-)to the clodronate liposomes group (Clodronate Group, n=7) and the vehicle liposomes group (Control Group, n=7). Clodronate (0.1 mL/10 g) was injected via the tail vein starting 2 days (d-2) before left common carotid artery injury. Results: The percentage of blod monocytes was subsequently decreased after clodronate injection (14.0± 7.4% at baseline, 6.8± 4.9% at 24 hours and 0.7± 0.3% at 1 wek after the clodronate liposome injection). The percentage of macrophages in the plaque area was significantly lower in the clodronate group at week 2 (32.0± 6.5 vs. 68.7±7.6%, respectively, p<0.05) and at wek 4 (37.3± 8.5 vs. 62.6± 9.4%, respectively, p<0.05). The interleukin (IL)-6 and tumor necrosis factor (TNF)-α concentrations were significantly decreased in the clodronate group at wek 4 (12.3± 2.5 vs. 22.9± 3.5 pg/mL, respectively, p<0.05 for IL-6 and 16.6± 2.2 vs. 43.6± 6.1 pg/mL, respectively, p<0.05 for TNF-α). The plaque volume was significantly greater in the control group at week 2 (0.345± 0.063 vs. 0.153± 0.053 mm2, respectively, p<0.05) and at week 4 (0.320± 0.027 vs. 0.167± 0.070 mm2, respectively, p<0.05). Conclusion : Intravenous administration of clodronate liposomes depleted monocytes and macrophages, and so this reduced the inflammatory markers and neointimal formation in ApoE (-) mice.

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      참고문헌 (Reference)

      1 권진숙, "주령에 따른 쥐 경동맥 손상 모델에서의 신생내막 형성율의 차이" 대한심장학회 37 (37): 78-83, 2007

      2 이무용, "고콜레스테롤혈증 토끼에서 경피적 동맥 성형술 또는스텐트 삽입술 후 신생내막의 형성에서 대식세포의 영향" 대한심장학회 35 (35): 801-811, 2005

      3 Park, S.J., "Thalidomide as a potent inhibitor of neointimal hyperplasia after balloon injury in rat carotid artery" 24 : 885-891, 2004

      4 Wang, L., "Stent-mediated methylprednisolone delivery reduces macrophage contents and in-stent neointimal formation" 16 : 237-243, 2005

      5 Schober, A., "Stabilization of atherosclerotic plaques by blockade of macrophage migration inhibitory factor after vascular injury in apolipoprotein E-deficient mice" 109 : 380-385, 2004

      6 Farb, A., "Oral everolimus inhibits in-stent neointimal growth" 106 : 2379-2384, 2002

      7 Kim, D.W., "Novel oral formulation of paclitaxel inhibits neointimal hyperplasia in a rat carotid artery injury model" 109 : 1558-1563, 2004

      8 Danenberg, H.D., "Macrophage depletion by clodronate-containing liposomes reduces neointimal formation after balloon injury in rats and rabbits" 106 : 599-605, 2002

      9 Matsumoto, Y., "Long-term inhibition of Rhokinase suppresses neointimal formation after stent implantation in porcine coronary arteries: involvement of multiple mechanisms" 24 : 181-186, 2004

      10 van Rooijen, N., "Liposome mediated depletion of macrophages:mechanism of action, preparation of liposomes and applications" 174 : 83-93, 1994

      1 권진숙, "주령에 따른 쥐 경동맥 손상 모델에서의 신생내막 형성율의 차이" 대한심장학회 37 (37): 78-83, 2007

      2 이무용, "고콜레스테롤혈증 토끼에서 경피적 동맥 성형술 또는스텐트 삽입술 후 신생내막의 형성에서 대식세포의 영향" 대한심장학회 35 (35): 801-811, 2005

      3 Park, S.J., "Thalidomide as a potent inhibitor of neointimal hyperplasia after balloon injury in rat carotid artery" 24 : 885-891, 2004

      4 Wang, L., "Stent-mediated methylprednisolone delivery reduces macrophage contents and in-stent neointimal formation" 16 : 237-243, 2005

      5 Schober, A., "Stabilization of atherosclerotic plaques by blockade of macrophage migration inhibitory factor after vascular injury in apolipoprotein E-deficient mice" 109 : 380-385, 2004

      6 Farb, A., "Oral everolimus inhibits in-stent neointimal growth" 106 : 2379-2384, 2002

      7 Kim, D.W., "Novel oral formulation of paclitaxel inhibits neointimal hyperplasia in a rat carotid artery injury model" 109 : 1558-1563, 2004

      8 Danenberg, H.D., "Macrophage depletion by clodronate-containing liposomes reduces neointimal formation after balloon injury in rats and rabbits" 106 : 599-605, 2002

      9 Matsumoto, Y., "Long-term inhibition of Rhokinase suppresses neointimal formation after stent implantation in porcine coronary arteries: involvement of multiple mechanisms" 24 : 181-186, 2004

      10 van Rooijen, N., "Liposome mediated depletion of macrophages:mechanism of action, preparation of liposomes and applications" 174 : 83-93, 1994

      11 Kang, D.H., "Inhibition of neointimal hyperplasia by external radiation in rat carotid injury model: the possible role of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1" 29 : 944-955, 1999

      12 이종민, "Inhibition of Neointima Formation by Anti-Vascular Endothelial Growth Factor and Receptor-1 Peptides in a Balloon-Injured Rat Carotid Artery" 대한심장학회 37 (37): 475-482, 2007

      13 Libby, P., "Inflammation in atherosclerosis" 420 : 868-874, 2002

      14 Wang, Y.X., "Increased aortic stiffness assessed by pulse wave velocity in apolipoprotein E-deficient mice" 278 : H428-H434, 2000

      15 Mori, E., "Essential role of monocyte chemoattractant protein-1 in development of restenotic changes (neointimal hyperplasia and constrictive remodeling) after balloon angioplasty in hypercholesterolemic rabbits" 105 : 2905-2910, 2002

      16 Qian, Q., "Elimination of mouse splenic macrophages correlates with increased usceptibility to experimental disseminated candidiasis" 152 : 5000-5008, 1994

      17 Schober, A., "Deposition of platelet RANTES triggering monocyte recruitment requires P-selectin and is involved in neointima formation after arterial injury" 106 : 1523-1529, 2002

      18 Wang, Y.X., "Cardiovascular functional phenotypes and pharmacological responses in apolipoprotein E deficient mice" 26 : 309-316, 2005

      19 Hancock, W.W., "CD4+ mononuclear cells induce cytokine expression, vascular smooth muscle cell proliferation, and arterial occlusion after endothelial injury" 145 : 1008-1014, 1994

      20 Labarrere, C.A., "C-reactive protein: from innocent bystander to pivotal mediator of atherosclerosis" 117 : 499-507, 2004

      21 Ross, R., "Atherosclerosis: an inflammatory disease" 340 : 115-126, 1999

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      학술지 이력

      학술지 이력
      연월일 이력구분 이력상세 등재구분
      2023 평가예정 해외DB학술지평가 신청대상 (해외등재 학술지 평가)
      2020-01-01 평가 등재학술지 유지 (해외등재 학술지 평가) KCI등재
      2011-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2009-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2008-05-15 학회명변경 한글명 : 대한순환기학회 -> 대한심장학회
      영문명 : The Korean Society Of Circulation -> The Korean Society of Cardiology
      KCI등재
      2007-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2005-08-02 학술지등록 한글명 : Korean Circulation Journal
      외국어명 : Korean Circulation Journal
      KCI등재
      2004-01-01 평가 등재학술지 선정 (등재후보2차) KCI등재
      2003-01-01 평가 등재후보 1차 PASS (등재후보1차) KCI등재후보
      2001-07-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
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      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 1.13 0.34 0.71
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.45 0.36 0.52 0.12
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