Pre-B cell colony enhancing factor (PBEF)/visfatin induces secretion of MCP-1 in human endothelial cells : role in visfatin-induced angiogenesis
Adya, Raghu, Tan, Bee K., Chen, Jing and Randeva, Harpal S.. (2009) Pre-B cell colony enhancing factor (PBEF)/visfatin induces secretion of MCP-1 in human endothelial cells : role in visfatin-induced angiogenesis. Atherosclerosis, Vol.205 (No.1). pp. 113-119. ISSN 0021-9150Full text not available from this repository.
Official URL: http://dx.doi.org/10.1016/j.atherosclerosis.2008.1...
Objectives: Visfatin and Monocyte-Chemoattractant-Protein-1 (MCP-1) are elevated in cardiovascular pathologies, insulin-resistant and diabetic states. Visfatin has been reported to exhibit pro-angiogenic actions in human endothelial cells. Given MCP-1's well described pro-angiogenic properties we sought to study the potential interaction between visfatin and MCP-1 in human endothelial cells. We also explored the possible autocrine/paracrine mechanisms governing this potential interaction; specifically we looked at the effect of visfatin on MCP-1's putative receptor (CCR2 receptor) in human endothelial cells.
Methods and results: Using in vitro angiogenic assays (capillary tube formation and migration), Western blotting and RT-PCR, we found that visfatin, dose-dependently, induced MCP-1 as well as CCR2 levels. We also studied the involvement of PI3Kinase, MAPKinase and NF-kappa B pathways in visfatin induced MCP-1/CCR2 levels by employing LY294002, U0126 and BAY11-7085, respectively. We found the increase in MCP-1 and CCR2 levels by visfatin were negated by LY294002 and BAY11-7085, but notwith U0126, suggesting the crucial role of PI3Kinase and NF-kappa B pathways in visfatin induced MCP-1 and its autocrine regulation via the CCR2 receptor. Finally, we consolidate the role of MCP-1 in visfatin-induced angiogenesis by employing CCR2 antagonist (RS-102895) and MCP-1 neutralising antibody, respectively.
Conclusions: Our novel data reveal that MCP-1 is pivotal in modulating visfatin-induced angiogenesis via NF-kappa B and PI3Kinase pathways. Furthermore, our findings elucidate the potential influence of autocrine/paracrine mechanisms (via the CCR2 receptor) underlying visfatin's angiogenic effects through MCP-1. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
|Item Type:||Journal Article|
|Subjects:||R Medicine > RC Internal medicine|
|Divisions:||Faculty of Medicine > Warwick Medical School > Biomedical Sciences > Translational & Experimental Medicine > Metabolic and Vascular Health (- until July 2016)
Faculty of Medicine > Warwick Medical School
|Journal or Publication Title:||Atherosclerosis|
|Publisher:||Elsevier Ireland Ltd.|
|Official Date:||July 2009|
|Number of Pages:||7|
|Page Range:||pp. 113-119|
|Access rights to Published version:||Restricted or Subscription Access|
|Funder:||University of Warwick|
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