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作 者:李海清[1] 赵强[1] 孙晓宁[2] 叶晓峰[1]
机构地区:[1]上海交通大学附属瑞金医院心脏外科,200025 [2]复旦大学附属中山医院心脏外科
出 处:《中华实验外科杂志》2009年第11期1407-1409,共3页Chinese Journal of Experimental Surgery
摘 要:目的探讨17β-雌二醇对小鼠骨髓源性内皮祖细胞(BM—EPCs)迁移功能的影响及其机制。方法培养卵巢切除BALB/C小鼠BM—EPCs。分别采用0、1、10、100nmol/L17β-雌二醇或相应浓度17β-雌二醇和雌激素受体拮抗剂ICI182 780与BM—EPCs共培养。48h后,Transwell小室检测BM—EPCs经或未经CXCR4抑制剂AMD3100处理后向基质细胞衍生因子-1α(SDF—1α)的迁移功能。逆转录-聚合酶链反应(RT—PCR)和流式细胞术检测各组BM—EPCs CXCR4的表达。结果17β-雌二醇呈剂量依赖性促进BM—EPCs迁移(0nmol/L:80.33±6.02;1nmol/L:110.67±7.51;10nmol/L:139.67±9.50;100nmol/L:168.00±10.00/400倍视野,P〈0.05)以及CXCR4 mRNA(CXCR4/β-actin:0nmol/L:0.091±0.007;1nmol/L:0.189±0.009;10nmol/L:0.208±0.006;100nmol/L:0.235±0.009,P〈0.05)和蛋白[CXCR4阳性率:0nmol/L:(29.57±4.20)%;1nmol/L:(49.23±6.01)%;10nmol/L:(64.69±4.46)%;100nmol/L:(75.59±4.88)%,P〈0.05]的表达,但被雌激素受体拮抗剂ICI182780完全阻断(P〉0.05)。结论17β-雌二醇通过雌激素受体途径上调BM—EPCs CXCR4的表达而增强其迁移功能。Objective To explore the effects and mechanisms of 17β-estradiol on the migratory capacity of bone marrow-derived endothelial progenitor cells (BM-EPCs). Methods BM-EPCs were cultured and identified from ovariectomized BALB/C mice tibia and femur. After 48-h coculture with 0,1,10, 100 nmol/L 17 β-estradiol, or, corresponding concentration of 17β-estradiol and estrogen receptors antagonist ICI182 780,BM-EPCs migratory capacity toward stromal cell-derived factor-1α was assessed by transwell chamber with or without treatment of CXCR4 inhibitor AMD3100, and the CXCR4 expression in BM-EPCs was detected by RT-PCR and FACS. Results Migratory capacity (0 nmol/L: 80.33 ± 6.02;1 nmol/L: 110.67 ±7.51 ;10 nmol/L:139.67 ±9.50;100 nmol/L:168.00 ± 10.00 per power fields) (P 〈0.05) and the CXCR4 expression [ CXCR4/β-actin :0 nmol/L :0.091 ± 0.007 ; 1 nmol/L :0.189 ± 0.009 ; 10 nmol/L : 0.208 ± 0. 006; 100 nmol/L: 0. 235 ± 0. 009,P 〈 0.05; CXCR4 positive rate:0 nmol/L: (29.57 ± 4.20)% ;1 nmol/L: (49. 23 ± 6. O1 )% ,10 nmol/L: (64. 69 ± 4. 46)% ; 100 nmo]/L: (75. 59 ± 4.88 )% ,P 〈 0. 05 ] in BM-EPCs were increased by 17β-estradiol in a dose-dependent manner, however, these effects were completely blocked by ICI182 780 (P 〉 0.05 ). Conclusion 17β-estradiol enhances migratory capacity of BM-EPCs by up-regulating the CXCR4 expression via estrogen receptors pathway.
分 类 号:R541.6[医药卫生—心血管疾病]
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