期刊文献+

兔后肢缺血诱导侧支血管生长过程中巨噬细胞浸润的变化 被引量:2

CHANGES OF MACROPHAGE INVASION DURING COLLATERAL VESSEL GROWTH INDUCED BY ISCHEMIA IN RABBIT HINDLIMB
下载PDF
导出
摘要 目的检测兔侧支血管生长过程中各时期巨噬细胞的浸润情况;方法单侧结扎兔后肢股动脉,随后将股动脉结扎的远侧端连到相邻的静脉上造成动静脉短路,另侧为对照组,分别存活2d,1周,2周,4周后处死,用特异性的巨噬细胞抗体(RAM11)免疫荧光组织化学结合共聚焦技术检测侧支血管壁内巨噬细胞的数目及其分布;结果在正常血管,其外膜有少量巨噬细胞的存在,股动脉结扎后2d,侧支血管外膜巨噬细胞的数目增加,并黏附至内皮细胞,结扎1周后,侧支血管外膜巨噬细胞的数目显著增加,中膜有巨噬细胞的浸润,结扎2周后,侧支血管外膜巨噬细胞的数目减少,但仍高于正常血管,结扎4周后,侧支血管巨噬细胞的数目明显减少,跟正常血管情况类似,统计学分析结果表明,在结扎后2d、一周、二周和四周不同的时间,巨噬细胞在侧支血管的分布差异具有显著性;结论侧支血管发育过程中巨噬细胞的浸润和侧支血管的形成密切相关,提示巨噬细胞参与了侧支血管的生长发育。 Objective To detect the change of macrophage invasion during collateral vessel growth.Methods Unilateral ligation in the rabbit hindlimb was followed by connecting the distal part of the ligated femoral artery to a nearby vein, causing artery-vein shunt. The other hindlimb served as control.The animals were killed after survival of 2d, 1week, 2weeks, and 4weeks respectively. The number and distribution of macrophages were detected by confocal immunofluorescence using the specific antibody against RAM11.Resu...
出处 《中国组织化学与细胞化学杂志》 CAS CSCD 2009年第1期40-43,共4页 Chinese Journal of Histochemistry and Cytochemistry
基金 湖南省教育厅科研基金资助项目(06C781 08C811)
关键词 巨噬细胞 侧支血管生长 结扎 Macrophage Collateral vessels Rabbit Ligation
  • 相关文献

参考文献2

  • 1Dimitri Scholz,Wei-jun Cai,Wolfgang Schaper. Arteriogenesis, a new concept of vascular adaptation in occlusive disease[J] 2001,Angiogenesis(4):247~257
  • 2M. Arras,R. Strasser,M. Mohri,R. Doll,P. Eckert,W. Schaper,J. Schaper. Tumor necrosis factor-alpha is expressed by monocytes/macrophages following cardiac microembolization and is antagonized by cyclosporine[J] 1998,Basic Research in Cardiology(2):97~107

同被引文献13

  • 1Vestweber D. VE-cadherin: the major endothelial adhesion molecule controlling cellular junctions and blood vessel formation [J]. Arterioscler Thromb Vasc Biol, 2008, 28(2): 223-232.
  • 2Dejana E, Toumier-Lasserve E,Weinstein BM. The control of vascular integrity by endothelial cell junctions: molecular basis and pathological implications[J]. Dev Cell, 2009, 16(2):209-221.
  • 3Vandenbroucke E, Mehta D, Minshail R, et al. Regulation of endothelial junctional permeability[J]. Ann N Y Acad Sci, 2008, 1123(1): 134-145.
  • 4Dejana E, Orsenigo F, Lampugnani MG. The role of adherens junctions and VE-cadhcrin in the control of vascular permeability [J]. J Cell Sci, 2008, 121(13): 2115-2122.
  • 5Harris ES,Nelson WJ. VE-cadhorin: at the front, center, and sides of endothelial cell organization and function[J]. Curt Opin Cell Biol,2010, 2(5):651-658..
  • 6Wallez Y, Huber P. Endothelial adherens and tight junctions in vascular homeostasis, inflammation and angioganesis [J]. Bioehim Biophys Acta, 2008, 1778(3):794-809.
  • 7Corada M, Mariotti M, Thurston G, et al. Vascular endothelial-eadherin is an important determinant of mierovaseular integrity in vivo [J]. Proc Natl Acad Sci U S A, 1999, 96(17):9815-9820.
  • 8Gonzalez D, Herrera B, Beltran A, et al. Nitric oxide disrupts VE-cadherin complex in murine microvaseular endothelial cells [J]. Bioehem Biophys Res Commun, 2003, 304(1):113-118.
  • 9Gotsch U, Borges E, Bosse R, et al. VE-cadherin antibody accelerates neutrophil recruitment in vivo[J]. J Cell Sci, 1997, 110 ( Pt 5):583-588.
  • 10Di Lorenzo A, Femandez-Hemando C, Cirino G, et al. Aktl is critical for acute inflammation and histamine-mediated vascular leakage[J]. Proc Natl Acad Sci U S A, 2009, 106(34):14552- 14557.

引证文献2

二级引证文献2

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部