期刊文献+

Effects of AMD3100 subconjunctival injection on alkali burn induced corneal neovascularization in mice 被引量:2

Effects of AMD3100 subconjunctival injection on alkali burn induced corneal neovascularization in mice
原文传递
导出
摘要 AIM: To investigate the therapeutic effects of local and systemic administration of AMD3100 for alkali burn induced corneal neovascularization (CNV) in mice. METHODS: CNV was induced in vivo by alkaline burn of cornea in C57BL/6 mice. AMD3100 was administrated topically by subconjunctival injection or systemically by intraperitoneal injection for 7 days; balanced salt solution was administrated topically or systemically as a control respectively. Inflammatory index was evaluated by slit-lamp biomicroscopy and inflammatory cells infiltrated to cornea tissue were detected by histologic analysis at multiple time points. CNV was compared between the local and systemic treated mice 2 weeks after alkali burn, as quantified by CD34 immunostaining. Fluorescence-Activated Cell Sorter Analysis was used to investigate the mobilizing effects of EPC in mice after subconjunctival injected or intraperitoneal injected AMD3100. Immunohistochemistry was used to detect the expression of endothelial progenitor cells (EPC) marker proteins VEGFR2 and CD34. RESULTS: Three days after alkali burn, infiltration of inflammatory cells was found in corneal tissue. At the first 7 days of local injection group, the number of inflammatory cells was significantly lower than that in systemic injection group. CNV could be seen at the 7(th) day, and at the 14(th) day reached the peak, then started to decrease. The number of CNV in the subconjunctival injection group was 7.57 +/- 1.26 per 0.034mm(2), compared to a number of 14.87 +/- 2.21 per 0.034mm(2) in the control group (P<0.05). On the contrary, the number of CNV in the intraperitoneal injection group was a little higher than that in the control group, 16.34 +/- 1.53 per 0.034mm(2) vs 13.26 +/- 1.87 per 0.034mm(2). The research also showed that intraperitoneally, but not subconjunctivally injected AMD3100 could mobilize EPC. On the other hand, subconjunctival, but not intraperitoneally injected AMD3100 could reduce the expression of EPC marker proteins. CONCLUSION: In mice locally administrated AMD3100 can reduce the number of alkali burn induced CNV. The number of inflammatory cells and inflammatory responses in corneal tissue. AIM: To investigate the therapeutic effects of local and systemic administration of AMD3100 for alkali burn induced corneal neovascularization (CNV) in mice. METHODS: CNV was induced in vivo by alkaline burn of cornea in C57BL/6 mice. AMD3100 was administrated topically by subconjunctival injection or systemically by intraperitoneal injection for 7 days; balanced salt solution was administrated topically or systemically as a control respectively. Inflammatory index was evaluated by slit-lamp biomicroscopy and inflammatory cells infiltrated to cornea tissue were detected by histologic analysis at multiple time points. CNV was compared between the local and systemic treated mice 2 weeks after alkali burn, as quantified by CD34 immunostaining. Fluorescence-Activated Cell Sorter Analysis was used to investigate the mobilizing effects of EPC in mice after subconjunctival injected or intraperitoneal injected AMD3100. Immunohistochemistry was used to detect the expression of endothelial progenitor cells (EPC) marker proteins VEGFR2 and CD34. RESULTS: Three days after alkali burn, infiltration of inflammatory cells was found in corneal tissue. At the first 7 days of local injection group, the number of inflammatory cells was significantly lower than that in systemic injection group. CNV could be seen at the 7(th) day, and at the 14(th) day reached the peak, then started to decrease. The number of CNV in the subconjunctival injection group was 7.57 +/- 1.26 per 0.034mm(2), compared to a number of 14.87 +/- 2.21 per 0.034mm(2) in the control group (P<0.05). On the contrary, the number of CNV in the intraperitoneal injection group was a little higher than that in the control group, 16.34 +/- 1.53 per 0.034mm(2) vs 13.26 +/- 1.87 per 0.034mm(2). The research also showed that intraperitoneally, but not subconjunctivally injected AMD3100 could mobilize EPC. On the other hand, subconjunctival, but not intraperitoneally injected AMD3100 could reduce the expression of EPC marker proteins. CONCLUSION: In mice locally administrated AMD3100 can reduce the number of alkali burn induced CNV. The number of inflammatory cells and inflammatory responses in corneal tissue.
出处 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2011年第1期44-48,共5页 国际眼科杂志(英文版)
关键词 alkali burn corneal neovascularization AMD3100 inflammatory cells EPC alkali burn corneal neovascularization AMD3100 inflammatory cells EPC
  • 相关文献

参考文献9

  • 1尹扬光,黄岚,赵晓辉,方玉强,周健,赵景红,陈剑飞,崔斌.SDF-1对小鼠骨髓源性内皮祖细胞数量及功能的影响[J].心血管康复医学杂志,2006,15(5):427-430. 被引量:12
  • 2Magda Kucia,Kacper Jankowski,Ryan Reca,Marcin Wysoczynski,Laura Bandura,Daniel J. Allendorf,Jin Zhang,Janina Ratajczak,Mariusz Z. Ratajczak.CXCR4–SDF-1 Signalling, Locomotion, Chemotaxis and Adhesion[J]. The Histochemical Journal . 2004 (3)
  • 3Ratajczak MZ,Zuba- Surma E,Kucia M,Reca R,Wojakowski W,Ratajczak J.The pleiotropic effects of the SDF- 1- CXCR4 axis in organogenesis,regeneration and tumorigenesis. Leukemia . 2006
  • 4Zhang Z,Ma JX,Gao G,Li C,Luo L,Zhang M,Yang W,Jiang A,Kuang W,Xu L,Chen J,Liu Z.Plasminogen kringle 5 inhibits alkali- burn- induced corneal neovascularization. Investigative Ophthalmology . 2005
  • 5Askari AT,Unzek S,Popovic ZB,Goldman CK,Forudi F,Kiedrowski M,Rovner A,Ellis SG,Thomas JD,DiCorleto PE,Topol EJ,Penn MS.Effect of stromal-cell-derived factor 1 on stem-cell homing and tissue regeneration in ischaemic cardiomyopathy. The Lancet . 2003
  • 6Myriam Grunewald,Inbal Avraham,Yuval Dor,et al.VEGF-induced adult neovascularization: recruitment, retention, and role of accessory cells. Cell . 2006
  • 7Walter DH,Haendeler J,Reinhold J, et al.Impaired CXCR4 signaling contributes to the reduced neovascularization capacity of endothelial progenitor cells from patients with coronary artery disease. Circulation Research . 2005
  • 8Y Yin,L Huang,X Zhao,Y Fang,S Yu,J Zhao,B Cui.AMD3100 mobilizes endothelial progenitor cells in mice, but inhibits its biological functions by blocking an autocrine/paracrine regulatory loop of stromal cell derived factor-1 in vitro. Journal of Cardiovascular Pharmacology . 2007
  • 9Gallagher KA,Liu ZJ,Xiao M, et al.Diabetic impairments in NO-mediated endothelial progenitor cell mobilization and homing are reversed by hyperoxia and SDF-la. The Journal of Clinical Investigation . 2007

二级参考文献7

  • 1赵晓辉,黄岚.内皮祖细胞生物学特性及其在心血管系统中的作用[J].中国介入心脏病学杂志,2005,13(6):405-407. 被引量:3
  • 2De Falco E,Porcelli D,Torella AR,et al.SDF-1 involvement in endothelial phenotype and ischemia-induced recruitment of bone marrow progenitor cells[J].Blood,2004,104:3472-3482.
  • 3Hiasa K,Ishibashi M,Ohtani K,et al.Gene transfer of stromal cell-derived factor-1 alpha enhances ischemic vasculogenesis and angiogenesis via vascular endothelial growth factor/endothelial nitric oxide synthase-related pathway:next-generation chemokine therapy for therapeutic neovascularization[J].Circulation,2004,109:2454-2461.
  • 4Werner N,Junk S,Laufs U,et al.Intravenous transfusion of endothelial progenitor cells reduces neointima formation after vascular injury[J].Circ Res,2003,93:17-24.
  • 5Walter DH,Rittig K,Bahlmann FH,et al.Statin therapy accelerate reendothelialization[J].Circulation,2002,105:3017-3024.
  • 6Yamaguchi J,Kusano KF,Masuo O,et al.Stromal cell-derived factor-1 effects on exvivo expanded endothelial progenitor cells recruitment for ischemic neovascularization[J].Circulation,2003,107:1322-1328.
  • 7Askari AT,Unzek S,Popovic ZB,et al.Effect of stromal cell-drived factor-1 on stem cell homing and tissue regeneration in ischemic cardiomyopathy[J].Lancet,2003,362:697-703.

共引文献17

同被引文献5

引证文献2

二级引证文献6

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