Facilitation of ultrasonic microvesicles on homing and molecular mechanism of bone marrow mesenchymal stem cells in cerebral infarction patients

被引:3
作者
Chang, F. [1 ]
Xiong, W. [1 ]
Wang, D. [1 ]
Liu, X. -Z. [1 ]
Zhang, W. [1 ]
Zhang, M. [1 ]
Jing, P. [1 ]
机构
[1] Huazhong Univ Sci & Technol, Cent Hosp Wuhan, Dept Neurol, Tongji Med Coll, Wuhan, Hubei, Peoples R China
关键词
Cerebral infarction; Ultrasonic microvesicle; Bone marrow mesenchymal stern cells; Homing; VEGF; ACUTE ISCHEMIC-STROKE; DIFFERENTIATION; THROMBOLYSIS; INJURY; MODEL;
D O I
暂无
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
OBJECTIVE: Cerebral infarction, or ischemia brain stroke, is a common cerebrovascular disease. Bone marrow mesenchymal stem cells (BMSCs) are widely used to treating ischemia disease such as cardiac infarction. Ultrasonic microvesicles may help the targeting of exogenous factors via localized energy blast. Therefore, this study aims to investigate the effect of ultrasonic microvesicles on the homing of BMSCs on artery thrombosis and the associated molecular mechanisms. MATERIALS AND METHODS: Rat BMSCs were isolated and cultured. Rats were divided into sham, model. BMSCs, and microvesicles groups. Cerebral infarction model was prepared by ligation of cervical artery and middle cerebral artery. 3x106/kg BMSCs were transplanted via tail veins. Microvesicles were used for assisting BMSCs infusion. Sex-determining region Y (SRY) gene expression was measured by Real-time PCR, while 2,3,5-triphenyltetrazolium chloride (TTC) staining was employed for describing the area of cerebral infarction. The activity of caspase 3 was assayed by test kit. Vascular endothelial growth factor (VEGF), nuclear factor kappa B (NE-kappa B) mRNA/protein levels, were quantified by Real-time PCR, and Western blotting, respectively. RESULTS: Microvesicle group had significantly elevated SRY expression (p<0.05 compared to BMSCs group). Transplantation of BMSCs remarkably decreased cerebral infarction area, caspase 3 activity or NE-kappa B expression, and increased VEGF expression (p<0.05 compared to model group). Microvesicle induced BMSCs had more potent effects (p<0.01). CONCLUSIONS: Ultrasound microvesicle facilitated homing of BMSCs in cerebral infarction, and improved infarction disease via up-regulating VEGF expression, inhibiting NE-kappa B expression, and modulating apoptosis.
引用
收藏
页码:3916 / 3923
页数:8
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