Correlation of CD34+ Cells with Tissue Angiogenesis after Traumatic Brain Injury in a Rat Model

Correlation of CD34+ Cells with Tissue Angiogenesis after Traumatic Brain Injury in a Rat Model
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DOI:
10.1089/neu.2008.0733
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发表时间:
2009-08-01
影响因子:
4.2
通讯作者:
Zhang, Jianning
Zhang, Jianning
中科院分区:
医学2区
文献类型:
--
作者:
Guo, Xinbin;Liu, Li;Zhang, Jianning

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被引文献

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越来越多的证据表明,循环内皮祖细胞(它是造血祖细胞CD34(+)细胞的一个亚群)在新生血管形成和组织修复中起着关键作用。我们在一个创伤性脑损伤(TBI)大鼠模型中验证了这样一个假设:创伤性脑损伤能够将CD34(+)细胞动员到外周血和脑组织中,这是血管修复的一个关键过程。雄性Wistar大鼠接受了可控性液压冲击。在创伤性脑损伤前后采集血液和脑组织,以测量外周血中CD34(+)细胞的水平,并检测它们在受损脑组织中的聚集情况。与手术对照组相比,创伤性脑损伤大鼠外周血中CD34(+)细胞显著增加,并在脑组织中聚集。免疫组织化学检测到具有不完全CD34(+)内皮样细胞衬里的新生血管,以及在损伤组织及其周围组织中微血管数量增加。结果表明,创伤性损伤后循环CD34(+)细胞的增加与创伤性脑损伤大鼠大脑中的血管生成密切相关。它们还表明,CD34(+)细胞移植或内源性CD34(+)细胞的增加可能是创伤性脑损伤患者的一种新的治疗方法。
Increasing evidence suggests that circulating endothelial progenitor cells, which are a subpopulation of hematopoietic progenitor CD34(+) cells, play a critical role in neovascularization and tissue repair. We have tested the hypothesis that traumatic brain injury (TBI) could mobilize CD34(+) cells to peripheral blood and brain tissue, a process critical for vascular repair, in a rat model of TBI. Male Wistar rats were subjected to controlled fluid percussion. Blood and brain tissue were collected before and after TBI to measure the levels of CD34(+) cells in peripheral blood and to detect their accumulation in the damaged cerebral tissue. Compared with surgery controls, CD34(+) cells significantly increased in the peripheral blood and accumulated in the brain tissue of TBI rats. Immunohistochemistry detected new vessels with incomplete CD34(+) endothelial-like cell lining and an increased number of microvessels in the injured and surrounding tissue. The results demonstrate a close correlation between an increase in circulating CD34(+) cells in response to traumatic injury and angiogenesis in TBI rat brain. They also suggest that transplantation of CD34(+) cells or augmentation of endogenous CD34(+) cells may be a novel therapeutic approach for patients with TBI.