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AGEs通过SDF-1/CXCR4轴信号通路对心肌微血管内皮细胞血管新生的影响及机制 被引量:3

Effect of AGEs on microvascular endothelial-cells angiogenesis by SDF-1/CXCR4 axis signaling pathway
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摘要 目的:探讨AGEs通过刺激SDF-1/CXCR4轴信号系统对心肌微血管内皮细胞的增值、迁移、管样结果形成的影响以及AMD3100对其的干预作用。方法:用不同浓度的AMD3100作用于浓度为200mg/L的AGEs共孵育的CMECs24h,用MTT法检测细胞活力及增殖能力,并选择合适的干扰浓度(抑制效果居中)。随机选取加入AGEs200ml/L的CMECs,加入合适浓度的AMD3100,分别作用24、48、72h,采用MTT法测定AGEs处理前后细胞增值率的变化,并检测AMD3100对增值率的影响;毛细血管管腔样结构形成实验检测对CMECs血管新生的影响和AMD3100对其阻断作用的影响。结果:心肌微血管内皮细胞增殖能力和迁移能力在24h、48h、72h有显著增强;并促进了心肌微血管内皮细胞管样形成(vsP<0.05);CXCR4受体阻断剂AMD3100作用于细胞后,可以显著阻断AGEs对心肌微血管内皮细胞增殖能力和迁移能力和管腔形成(vsP<0.05)的影响。结论:AGEs在早期显著增强了心肌微血管内皮细胞的增殖、迁移和管样结构形成的能力,其作用机制可能与SDF-1/CXCR4轴信号通路有关。 Objective:To observe the effects of the advanced glycation end products(AGEs) on proliferation,migration,angiogenesis and lumen formation of cardiac microvascular endothelial cells(CMECs) by SDF-1/CXCR4 axis signaling pathway.Method:Add different concentrations of AMD3100 to CMECs incubated with AGEs 9200mg/L) for 24h.MTT were used to detect the cell viability and proliferation.Ac-cording to the results,chose a concentration for next experiment.AGEs with the CXCR4 blocker AMD3100 1ng/mL were added with CMECs of 24h、48h、72h,Then,proliferation and migration were detected by MTT and transwell.Capillary lumen formation test was applyed to detect the angiogenesis.Result:CMECs in the AGEs concentration of 200 mg/L after 24h、48h、72h incubation,the A values were 0.1067 ±0.0113;0.1422 ±0.0058;0.1855 ±0.0225,which significantly higher than 0.0883 ±0.0233;0.1075±0.0184;0.1397±0206(P0.01);and tubule-like formation structure of CMECs were 3.416±0.791,4.737±1.129,7.470±1.890 higher than 2.227±0.6149,2.716±1.186,3.487±1.722)m/m2(P0.05 vs.control group).All of those showed time-dependent.CONCLUSION:AGEs ad-vanced proliferation,migration and tubule-like structure formation with time-dependent and.can enhance the proliferation,migration,angiogenesis and lumen formation of cardiac microvascular endothelial cells(CMECs) by SDF-1/CXCR4 axis sinnaling pathway.Conclusion:AGEs were significantly increased in the early cardiac microvascular endothelial cell proliferation,migration and lumen forma tion capabilities,and its mechanism may be related to SDF-1/CXCR4 axis pathway.
出处 《现代生物医学进展》 CAS 2010年第7期1270-1272,共3页 Progress in Modern Biomedicine
关键词 糖基化终产物 基质细胞衍生因子-1 CXCR4 心肌微血管内皮细胞 管腔结构 AGEs SDF-1 CXCR4 cardiac microvascular endothelial cell tube formation
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参考文献9

  • 1De-Falco E, PorcelliD, TorellaA R,et al. SDF-1 involvement in endothelial phenotype and ischemia-induced recruitment of bone marrow progenitor cells[J]. Blood, 2004, 104(12): 3472-3482.
  • 2FlomenbergN, DiPersio J, CalandraG. Role ofCXCR4 chemokine re-ceptor blockade usingAMD3100 formobilization of autologous hematopoietic progenitor cells [J]. Acta Haemato,l 2005, 114 (4): 198-199.
  • 3杨启红,徐强,司良毅.糖基化终产物对单核细胞源性巨噬细胞过氧化物酶体增殖物激活型受体γ表达的影响[J].中华老年心脑血管病杂志,2008,10(3):214-217. 被引量:4
  • 4尹志勇,魏丽萍,郝媛媛,张荣庆,李聪叶,王海昌.LY333531对高糖所致心肌微血管内皮细胞通透性上调的拮抗作用[J].细胞与分子免疫学杂志,2009,25(4):303-305. 被引量:11
  • 5Raza JA,Movahed A. Current concepts of cardiovascular disease in diabetes mellitus[J]. Int J Cardiol,2003,89:123-134.
  • 6Takeuchi M,Yamagishi S. Possible involvement of advanced glyeation end-products (AGEs) in the pathogenesis of Alzheimer's disease[J]. Curr Pharm Des, 2008, 14(10):973-978.
  • 7Huijberts MS, Schaper NC, Schalkwijk CG. Advanced glycation end products and diabetic foot disease[J]. Diabetes Metab Rcs Rev, 2008, 24(Suppl 1):S19-S24.
  • 8Yamaguchi J, KusanoK F, MasuoO,etal. Stromal cell-derived fae-or-1 effects onex vivoexpanded endothelial progenitor cell recruitment for ischemic neovascularization[J]. Circulation, 2003, 107(9): 1322-1328.
  • 9SalvucciO,Yao L,Villalba S, et a.1 Regulation of endothelial cell- branchingmorphogenesis by endogenous chemokine stromal-derived factor-1 [J]. Blood, 2002, 99:2703-2711.

二级参考文献22

  • 1王浩,叶平.过氧化物酶体增殖物激活型受体γ激活剂噻唑烷二酮类药物与心肌缺血再灌注损伤[J].中华老年心脑血管病杂志,2006,8(9):639-640. 被引量:1
  • 2Bates DO, Hillman NJ, Williams B, et al. Regulation of microvascular permeability by vascular endothelial growth factors [J]. J Anat, 2002, 200(6) : 581 -597.
  • 3Arikawa E, Ma RC, Isshiki K, et al. Effects of insulin replacements, inhibitors of angiotensin, and PKCbeta's actions to normalize cardiac gene expression and fuel metabolism in diabetic rats [ J]. Diabetes, 2007, 56(5) : 1410 -1420.
  • 4Xia Z, Kuo KH, Nagareddy PR, et al. N-acetylcysteine attenuates PKCbeta2 overexpression and myocardial hypertrophy in streptozotocin-induced diabetic rats[J].Cardiovasc Res, 2007, 73 (4) : 770 - 782.
  • 5Ishii H, Jirousek MR, Koya D, et al. Amelioration of vascular dysfunctions in diabetic rats by an oral PKC beta inhibitor[ J]. Science, 1996, 272 (5262) : 728 - 731.
  • 6Aiello LP, Davis MD, Girach A, et al. Effect of ruboxistaurin on visual loss in patients with diabetic retinopathy [ J ]. Ophthalmology, 2006, 113(12) : 2221 -2230.
  • 7Tuttle KR, Bakris GL, Toto RD, et al. The effect of ruboxistaurin on nephropathy in type 2 diabetes [ J ], Diabetes Care, 2005, 28 ( 11 ) : 2686 - 2690.
  • 8Wu Y, Wu G, Qi x, et al. Protein kinase C beta inhibitor LY333531 attenuates intereellular adhesion molecule-1 and monoeyte ehemotaetie protein-1 expression in the kidney in diabetie rats [ J ]. J Pharmacol Sci, 2006, 101(4) : 335 -343.
  • 9Li AC, Brown KK, Silvestre MJ, et al. Peroxisome proliferators activated receptor gamma ligands inhibit development of atherosclerosis in LDL receptor-deficient mice. J Clin Invest,2000,106:523-531.
  • 10Chen Z,Tshibashi S,Perry S, et al. Troglitazone inhibits atherosclerosis in apolipoprotein E-knockout mice: pleiotropic effects on CD36 expression and HDL. Arterioscler Thromb Vase Biol,2001,21:372-377.

共引文献11

同被引文献45

  • 1Vlassara H.Recent progress in advanced glycation endproducts andiabetic complications[J].Diabetes,1997,46(2):S19-S25
  • 2Nemir M,Pedrazzini T.Functional role of Notch signaling in thedeveloping and postnatal heart[J].J Mol Cell Cardiol,2008,45(4):495-504
  • 3Staton CA,Stribbling SM,Tazzyman S,et a1.Current methods assaying angiogenes is in vitro and in vivo[J].Int J Exp Pathol,2004,85(5):233-248
  • 4Aneia A,Tang WH,Bansilal S,et a1.Diabetic Cardiomyopathy:Insights into pathogenesis,diagnostic challenges and therapeuticoptions[J].Am J Med,2008,121(9):748-757
  • 5Takeuchi M, Yamagishi S. Possible involvement of advanced glycation end-products (AGEs)in the pathogenesis of Alzheimer'S diseasel [J]. Curr Pharm Des,2008,14(10):973-978.
  • 6Peppa M,Uribarri J,Vlassara H.The role of advanced glycation endproducts in the development of atherosclerosis[J].Curr Diabed Rep,2004,4(1):31-36
  • 7Bucala R.Recent Progress in advanced glycation and diabetic vasc-ular disease:role of advanced glycation end product receptors[J].Diabetes,1996,45:65-66
  • 8Hayat SA,Patel B,Khattar RS,et a1.Diabetic cardiomyopathy:Mechanisms,diagnosis and treatment[J].Clin Sci(Lond),2004,107:539-557
  • 9Huijberts MS,Schaper NC,Schalkwijk CG.Advanced glycation endproducts and diabetic foot disease[J].Diabetse Metab Res Rev,2008,24(1):S19-S24
  • 10Niessen K,Karsan A.Notch signaling in the developing cardiovas-cular system[J].Am J Physiol Gell Physiol,2007,293:C1-C11

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