肝细胞生长因子
血管内皮生长因子
脊髓损伤
医学
胎盘生长因子
生长因子
血管生成
新生血管
血小板衍生生长因子
转化生长因子
内科学
内分泌学
脊髓
血小板源性生长因子受体
病理
男科
受体
血管内皮生长因子受体
精神科
作者
Marie‐Françoise Ritz,Ursula Graumann,Bertha Gutierrez,Oliver Hausmann
出处
期刊:Current Neurovascular Research
[Bentham Science]
日期:2010-11-01
卷期号:7 (4): 301-310
被引量:28
标识
DOI:10.2174/156720210793180756
摘要
Traumatic spinal cord injury (SCI) disrupts the blood-spinal cord barrier and reduces the blood supply caused by microvascular changes. Vessel regression and neovascularization have been observed in the course of secondary injury contributing to microvascular remodeling after trauma. Spatio-temporal distribution of blood vessels and modulation of gene expression of several angiogenic factors have been investigated in rats after spinal cord compression injury. Rarefaction of vessels was detectable at the injury site 2 days after SCI before they disappeared in the developing cavity after 2 and 4 weeks, whereas no changes were observed in the penumbra. Investigation of the temporal expression of angiogenic genes using quantitative RT-PCR disclosed a constant down-regulation of the vascular endothelial growth factor (VEGF), and transient decreases of angiopoietin-1 (Ang-1), platelet-derived growth factor-BB (PDGF-BB), as well as placental growth factor (PlGF), with the lowest values obtained 3 days after injury, when compared to the expression levels obtained in sham-operated rats. Hepatocyte growth factor (HGF) was the only angiogenic factor with a constant increased gene expression when compared with controls, starting at day 3 post-SCI. mRNA levels of transforming growth factor-beta 1 (TGF-β1) were elevated at every time point following SCI, whereas those encoding for the cysteine-rich protein CCN1/CYR61 were upregulated after 2 h, 6 h, and 1 week only. Our data provide an overview of the temporal modulated expression of the major angiogenic factors, hampering revascularization in the lesion during the phase of secondary injury. These findings should be considered in order to improve therapeutic interventions.
科研通智能强力驱动
Strongly Powered by AbleSci AI