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Pre-B cell colony enhancing factor (PBEF)/visfatin induces secretion of MCP-1 in human endothelial cells : role in visfatin-induced angiogenesis
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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. doi:10.1016/j.atherosclerosis.2008.11.024 ISSN 0021-9150.
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Official URL: http://dx.doi.org/10.1016/j.atherosclerosis.2008.1...
Abstract
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 Science, Engineering and Medicine > Medicine > Warwick Medical School > Biomedical Sciences > Translational & Experimental Medicine > Metabolic and Vascular Health (- until July 2016) Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School |
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| Journal or Publication Title: | Atherosclerosis | ||||
| Publisher: | Elsevier Ireland Ltd. | ||||
| ISSN: | 0021-9150 | ||||
| Official Date: | July 2009 | ||||
| Dates: |
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| Volume: | Vol.205 | ||||
| Number: | No.1 | ||||
| Number of Pages: | 7 | ||||
| Page Range: | pp. 113-119 | ||||
| DOI: | 10.1016/j.atherosclerosis.2008.11.024 | ||||
| Status: | Peer Reviewed | ||||
| Publication Status: | Published | ||||
| Access rights to Published version: | Restricted or Subscription Access | ||||
| Funder: | University of Warwick |
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