These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: C-reactive protein promotes adhesion of monocytes to endothelial cells via NADPH oxidase-mediated oxidative stress.
    Author: Huang X, Zhang J, Liu J, Sun L, Zhao H, Lu Y, Wang J, Li J.
    Journal: J Cell Biochem; 2012 Mar; 113(3):857-67. PubMed ID: 22020763.
    Abstract:
    Enhanced monocyte adhesion to endothelial cells is an early event in atherogenesis. It has been shown that C-reactive protein (CRP) plays a key role in atherogenesis. Here, we investigated the effects of CRP on monocyte-endothelial cell adhesion and tested the hypothesis that NADPH oxidase (NOX)-mediated oxidative stress might play a key role in CRP-induced monocyte-endothelial cell adhesion. Firstly, 36 patients with carotid intima-media thickness (IMT) incrassation and 34 controls were enrolled in this study. The levels of glucose, lipids, CRP, monocyte chemotractant protein (MCP-1), malondialdehyde (MDA), and protein carbonylation were analyzed. The results showed that carotid IMT was associated with abnormal lipid metabolism, including elevated CRP, triglycerides (TG) (P < 0.01) and decreased high density lipoprotein (HDL) level (P < 0.05). The levels of CRP and MCP-1 in patients with carotid IMT incrassation were increased compared with the controls (P < 0.01). Moreover, patients with carotid IMT incrassation displayed enhanced MDA and protein carbonylation levels (P < 0.01), accompanied by activation and up-regulation of NOX in monocytes (P < 0.05) compared with the controls. The monocytes isolated from five healthy donors were used for in vitro experiments. Reactive oxygen species (ROS) production and NOX expression in monocytes were examined. The results also indicated that CRP could promote the adhesion of monocyte-endothelial cell by up-regulation of MCP-1 expression (P < 0.05). Importantly, NFκ B and p38 MAPK signaling pathways, which were activated by NOX-derived ROS, were involved in CRP-induced monocyte-endothelial cell adhesion and up-regulation of MCP-1 expression. These data suggested that CRP could promote the adhesion of monocytes to endothelial cells via NOX-mediated oxidative stress. J. Cell. Biochem. 113: 857-867, 2012. © 2011 Wiley Periodicals, Inc.
    [Abstract] [Full Text] [Related] [New Search]