首页 / 院系成果 / 成果详情页

Complement component C3a plays a critical role in endothelial activation and leukocyte recruitment into the brain 期刊论文

编号：

0ca61ca7-ae44-4252-b407-3ed6889e9702
作者：

Wu, Fengjiao^[1];Zou, Qiang^[2];Ding, Xiaodan^[1];Shi, Dongyan^[1];Zhu, Xingxing^[1];Hu, Weiguo(胡维国)^[3,4]Liu, Lixin^[5];Zhou, Hong^[1];
语种：

English
期刊：

JOURNAL OF NEUROINFLAMMATION ISSN：1742-2094 2016 年 13 卷 ; JAN 28
收录：
关键词：

Complement CNS inflammation Intravital microscopy Adhesion molecule Leukocyte recruitment
摘要：

Background: The complement system is becoming increasingly recognized as a key participant in many neurodegenerative diseases of the brain. Complement-deficient animals exhibit reduced neuroinflammation. Methods: In the present study, we administered intracerebroventricularly lipopolysaccharide (LPS) to mimic local infection of the brain and investigated the role of key complement component C3 in brain vasculature endothelial activation and leukocyte recruitment. The degree of neutrophil infiltration was determined by esterase staining. Leukocyte-endothelial interactions were measured using intravital microscopy. Cerebral endothelial activation was evaluated using real-time PCR and Western blotting. Results: Neutrophil infiltration into the brain cortex and hippocampus was significantly reduced in C3(-/-) mice and C3aR(-/-) mice but not in C6(-/-) mice. We detected markedly attenuated leukocyte-endothelial interactions in the brain microvasculature of C3(-/-) mice. Accordingly, in response to LPS administration, the brain microvasculature in these mice had decreased expression of P-selectin, E-selectin, intercellular cell adhesion molecule 1 (ICAM-1), and vascular cell adhesion molecule 1 (VCAM-1). Depletion of C3 from the circulation also caused reduction in VCAM-1 and Eselectin expression and leukocyte recruitment, suggesting that C3 in the circulation contributed to brain endothelial activation. Furthermore, C3(-/-) mice exhibited decreased leukocyte recruitment into the brain upon tumor necrosis factor-a (TNF-alpha) stimulation. C3a activated the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-kappa B) and induced the upregulation of VCAM-1 and ICAM-1 expression in murine primary cerebral endothelial cells in vitro. Conclusions: Our study provides the first evidence that C3a plays a critical role in cerebral endothelial activation and leukocyte recruitment during inflammation in the brain.
推荐引用方式
GB/T 7714：

Wu Fengjiao,Zou Qiang,Ding Xiaodan, et al. Complement component C3a plays a critical role in endothelial activation and leukocyte recruitment into the brain [J].JOURNAL OF NEUROINFLAMMATION,2016,13.
APA：

Wu Fengjiao,Zou Qiang,Ding Xiaodan,Shi Dongyan,&Zhou Hong.(2016).Complement component C3a plays a critical role in endothelial activation and leukocyte recruitment into the brain .JOURNAL OF NEUROINFLAMMATION,13.
MLA：

Wu Fengjiao, et al. "Complement component C3a plays a critical role in endothelial activation and leukocyte recruitment into the brain" .JOURNAL OF NEUROINFLAMMATION 13(2016).

浏览次数：25  下载次数：0

分享到：

浏览次数：25

下载次数：0

打印次数：0