激素性股骨头坏死患者中两种内皮祖细胞功能的改变

目的 观察激素性股骨头坏死患者外周血中两种内皮祖细胞功能的改变,探讨其在激素导致的内皮功能失调中的作用.方法 选择33例激素性股骨头坏死患者和33例性别与年龄相匹配的健康人,从外周血中分离培养早期内皮祖细胞(EPCs)和内皮集落形成细胞(ECFCs),体外培养并检测其集落形成能力、CCK-8检测增殖能力、Transwell小室检测迁移能力、Matrigel胶检测成血管能力、酶联免疫吸附试验( ELISA)检测血管内皮生长因子(VEGF)和基质细胞衍生因子(SDF) 1细胞因子分泌水平.结果 激素性股骨头坏死患者中的两种内皮祖细胞集落形成能力均有所下降[早期EPC集落数:2.42±1.46比4.52±2.00(P＜0.05)；ECFC集落数:0.62±0.55比1.12±0.82(P ＜0.05)],早期内皮祖细胞的迁移能力下降[63.8±11.7比152.3±12.4(P＜0.01)],分泌VEGF因子能力下降[(50.8±7.2) ng/L比(62.8±10.1)ng/L,P＜0.01],内皮集落形成细胞的增殖能力下降(P＜0.05),成血管能力下降[7.1±2.7比23.8±4.3(P＜0.01)].结论 激素性股骨头坏死患者中两种内皮祖细胞的功能在不同方面受损,表明其在激素导致的内皮功能失调中发挥不同作用.

Impairment of two types of circulating endothelial progenitor cells in patients with glucocorticoidinduced avascular osteonecrosis of the femoral head

Objective To investigate whether the functions of two types of endothelial progenitor cells (EPCs) were changed in glucocorticoid-induced avascular osteonecrosis of the femoral head (ANFH) and to explore the role they played in regional endothelial dysfunction.Methods Early EPCs and endothelial colony forming cells (ECFCs) obtained from 33 patients with glucocorticoid-induced ANFH and 33 ageand sex-matched control subjects were isolated,in vitro cultured and characterized by immunofluorescence.Colony forming units,growth kinetics,migratory capacity,tube formation capacity and cytokine levels in the supernatants of two types of EPCs were assayed in glucocorticoid-induced ANFH and control subjects.Results The number of EPCs colonies formed by two types of EPCs was decreased in glucocorticoid-induced ANFH patients (2.42 ± 1.46 colonies/well versus 4.52 ±2.00 colonies/well,P ＜0.05 and 0.62 ±0.55 colonies/well versus 1.12 ± 0.82 colonies/well,P ＜ 0.05,respectively).Early EPCs from ANFH patients showed impaired migratory capacity [ 63.8 ± 11.7 versus 152.3 ± 12.4 ( P ＜ 0.01 ) ] and VEGF secretion [ (50.8 ± 7.2) ng/L versus ( 62.8 ± 10.1 ) ng/L,P ＜ 0.01 ].ECFCs from glucocorticoid-induced ANFH patients showed impaired proliferation rate ( P ＜ 0.05) and tube formation capacity [ 7.1 ±2.7 versus 23.8 ±4.3 ( P ＜0.01 ) ].Conclusion The functions of both early EPCs and ECFCs were impaired in glucocorticoid-induced ANFH,and their distinct reduced capacity profiles may reflect different roles they played in regional endothelial dysfunction of glucocorticoid-induced ANFH.