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C反应蛋白对内皮祖细胞部分生物学功能的影响及其机制的实验研究 被引量:11

Effects of C-reactive protein on bone marrow-derived endothelial progenitor cell function
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摘要 目的观察C反应蛋白(CRP)对体外培养骨髓源性内皮祖细胞(EPC)数量及增殖、迁移、黏附功能的影响及其机制探讨。方法密度梯度离心法获取骨髓单个核细胞,FITC-荆豆凝集素I、DiI-乙酰化低密度脂蛋白荧光双染鉴定。单个核细胞培养7d后进行实验分组,分为对照组和CRP干预组。CRP干预组加入不同浓度CRP(分别为5、10、15、20μg/ml)培养48h,然后分别采用四氮唑溴盐比色法、改良的Boyden小室和黏附能力测定来观察EPC的增殖、迁移和黏附能力。RT-PCR检测不同浓度下CRP对EPC内皮型一氧化氮合酶(eNOS)mRNA的影响,并检测EPC的NOS活性。结果CRP(分别为5、10、15、20μg/ml)各组EPC数量分别为(58±3)、(54±3)、(47±3)和(39±5)个,对照组EPC数量为(60±3)个。MTT法检测CRP各亚组EPC在490nm吸光度值分别为0.332±0.003、0.297±0.036、0.273±0.013和0.259±0.035,对照组为0.345±0.014。CRP浓度为10、15、20μg/ml 3个亚组EPC的数量及增殖能力显著低(P〈0.01)。CRP各组(10、15、20μg/ml)与对照组相比EPC黏附数量明显低[(28±2)、(22±3)、(19±3)和(16±2)个比(30±2)个,P〈0.05]。不同浓度CRP各组与对照组相比EPC迁移数量明显低[(11±2)、(9±2)、(6±2)和(5±1)个比(12±2)个,P〈0.05]。CRP各亚组(5、10、15、20μg/ml)EPC eNOS mRNA相对光密度显著低于对照组。CRP呈剂量依赖性降低EPCNOS活性,CRP各组EPC的NOS活性分别为(66.29±1.81)、(57.44±3.25)、(48.37±3.86)和(36.82±4.89)nmol/mg蛋白,对照组EPCNOS活性为(68.56±2.82)nmol/mg蛋白,其中浓度为10、15、20μg/ml CRP组与对照组比较差异有统计学意义(P〈0.01)。结论CRP可能通过影响EPC eNOS表达活性降低EPC数量并影响其部分生物学功能。 Objective To observe the effects of C reactive protein (CRP) on endothelial progenitor cell (EPCs) function. Methods Mononuclear cells ( MNCs), isolated from bone marrow by density gradient centrifugation combined with adherent cell filtration, were plated on fibronectin coated culture dishes. After 7 days, adherent cells were cultured with different concentrations of CRP (0, 5,10, 15,20μg/ml) for 48 hours. EPCs prohferation and migration ability were observed and adhesion assay was performed. The eNOS mRNA expression of EPCs were measured by RT-PCR. Results The number of EPCs in C RP groups (10,15,20μg/ml) was obviously lower than that in control group (54±3,47±3,39±5 vs. 60±3,P 〈 0.01 ). EPCs proliferation capacity was inhibited in C RP groups ( 10,15,20μg/ml ) compared with that in control group (0.297±0.036,0.273±0.013,0.259±0.035 vs. 0.345±0.014,P〈0.01). EPCs migration capacity was inhibited significantly in CRP groups (5,10,15,20μg/ml) than that in control group ( 28±2, 22 ±3, 19±3,16±2 vs. 30±2, P 〈 0.05 ). EPCs adhensive number was lower in CRP groups than that in control group ( 11±2, 9±2, 6±2,5±1 vs. 12±2 ,P 〈 0.05 ). The mRNA expressions of eNOS in CRP groups were significantly lower in control group. And compared with control group, NOS activity decreased significantly in CRP groups ( 10,15,20μg/ml) ( 57.44±3.25,48.37±3.86,36.82±4. 89 vs. 68.56±2.82, P 〈 0.01 ). Coonclusion CRP could both reduce EPCs number and inhibit EPCs functions.
出处 《中华心血管病杂志》 CAS CSCD 北大核心 2008年第5期435-438,共4页 Chinese Journal of Cardiology
基金 基金项目:国家自然科学基金资助项目(30470729)
关键词 动脉粥样硬化 C反应蛋白质 干细胞 一氧化氮合酶 Atherosclerosis C-reactive protein Stem cells Nitric oxide synthase
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参考文献10

  • 1崔斌,黄岚,宋耀明,李爱民,晋军,覃军,于学军,耿召华,赵刚,周晓波.冠心病患者高敏C反应蛋白与循环内皮祖细胞的关系及临床意义[J].重庆医学,2005,34(9):1344-1346. 被引量:6
  • 2崔斌,黄岚,宋耀明,李爱民,晋军,覃军,于学军,耿召华.冠心病患者循环内皮祖细胞与相关危险因素及冠状动脉病变的关系[J].中华心血管病杂志,2005,33(9):785-788. 被引量:31
  • 3Lamping K. Endothelial progenitor cells: sowing the seeds for vascular repair. Circ Res ,2007,100 : 1243-1245.
  • 4Gertz K, Priller J, Kronenberg G, et al. Physical activity improves long-term stroke outcome via endothelial nitric oxide synthase- dependent augmentation of neovascularization and cerebral blood flow. Circ Res,2006,99 : 1132-1140.
  • 5Hoetzer GL, Irmiger HM, Keith RS, et al . Endothelial nitric oxide synthase inhibition does not alter endothelial progenitor cell colony forming capacity or migratory activity. J Cardiovasc Pharmacol,2005,46 : 387-389.
  • 6Iwakura A, Shastry S, Luedemann C, et al. Estradiol enhances recovery after myocardial infarction by augmenting incorporation of bone marrow-derived endothelial progenitor cells into sites of ischemia-indueed neovascularization via endothelial nitric oxide synthase-mediated activation of matrix metalloproteinase-9. Circulation ,2006,113 : 1605-1614.
  • 7Suh W, Kim KL, Choi JH, et al. C-reactive protein impairs angiogenic functions and decreases the secretion of arteriogenic chemo-cytokines in human endothelial progenitor cells. Biochem Biophys Res Commun, 2004,321:65-67.
  • 8Verma S, Kuliszewski MA, Li SH, et al. C-reactive protein attenuates endothelial progenitor cell survival, differentiation, and function : further evidence of a mechanistic link between C-reactive protein and cardiovascular disease. Circulation, 2004,109:2058- 2067.
  • 9Fujii H, Li SH, Szmitko PE, et al. C-reactive protein alters antioxidant defenses and promotes apoptosis in endothelial progenitor cells. Arterioscler Thromb Vasc Biol,2006, 26: 2476- 2482.
  • 10Schwartz R, Osborne-Lawrence S, Hahner L, et al. C-reactive protein downregulates endothelial NO synthase and attenuates reendothelialization in vivo in mice. Cir Res,2007, 100: 1405- 1407.

二级参考文献19

  • 1陈国伟 郑宗鄂.现代心脏病学[M].长沙:湖南科学技术出版社,1995.928.
  • 2Szmitko PE, Fedak PWM, Weisel RD, et al. Endothelial progenitor cells: new hope for a broken heart. Circulation, 2003,107:3093-3100.
  • 3Vasa M, Fichtlscherer S, Aicher A, et al. Number and migratory activity of circulating endothelial cells inversely correlate with risk factors for coronary artery disease. Circ Res, 2001, 89: e1-7.
  • 4Kalka C, Masuda H, Takahashi T, et al. Transplantation ofex vivo expanded endothelial progenitor cells for therapeutic neovascularization. Proe Natl Acad Sci USA, 2000,97:3422-3427.
  • 5Walter DH, Kilian Ritting, Ferdinand HB, et al. Statin therapy accelerates reendothelialization: a novel effect involving mobilization and incorporation of bone marrow derived endothelial progenitor cells. Circulation, 2002,105:3017-3024.
  • 6Mihail H, Wolfgang Erl, Peter CW, et al. Endothelial progenitor cells mobilization, differentiation, and homing. Arterioscler Thromb Vasc Biol, 2003,23 : 1185-1189.
  • 7Hill JM, Zalos G, Julian PJ, et al. Circulating endothelial progenitor cells , vascular function , and cardiovascular risk. N Engl J Med,2003,348:593-600.
  • 8Szmitko PE, Fedak PWM, Weisel RD, et al. Endothelial progenitor cells:new hope for a broken heart[J]. Circulation,2003,107:3093.
  • 9Morrow DA,Rifai N,Antman EM,et al.C reactive protein is a potent predictor of mortality independently of and in combination with troponin T in acute coronary syndromes: a TIMI ⅡA substudy[J].J Am Coll Cardio l,1998,31:1460.
  • 10Vasa M, Fichtlscherer S, Aicher A, et al. Number and migratory activity of circulating endothelial cells inversely correlate with risk factors for coronary artery disease[J].Circ Res, 2001, 89: e1.

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