OPG Expression on Endothelial Cells and Modulation by IL-1B, PDGF, Insulin, and Glucose
|Carmen Pérez de Ciriza1, Allan Lawrie2 and Nerea Varo1*|
|1Clinical Chemistry Department, Clínica Universidad de Navarra, Pamplona, Spain|
|2Cardiovascular Sciences, Royal Hallamshire Hospital, Sheffield, UK|
|Corresponding Author :||Nerea Varo
Servicio de Bioquímica, Clínica Universidad de Navarra
Avda Pío XII 36, 31008 Pamplona, Spain
Tel: 948 296 395
Fax: 948 296 500
E-mail: [email protected]
|Received: September 11, 2015; Accepted: September 30, 2015; Published: October 07, 2015|
|Citation: de Ciriza CP, Lawrie A, Varo N (2015) OPG Expression on Endothelial Cells and Modulation by IL-1B, PDGF, Insulin, and Glucose. Biochem Physiol 4:179. doi:10.4172/2168-9652.1000179|
|Copyright: © 2015 de Ciriza CP, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.|
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Introduction: Osteoprotegerin (OPG), an osteoclastogenesis inhibitor implicated in bone remodelling, has emerged as a potential biomarker for cardiovascular diseases. However, OPG circulating sources or the stimuli that increase its release and effects have not been established.
Objective: The aim of the present study are to establish whether endothelial cells may be a potential source of OPG, different mediators and OPG effects on endothelial cells.
Aim: The aim of the present study were: 1) to establish whether endothelial cells may be a potential source of circulating OPG, 2) to study induced OPG expression and release stimulated by different factors and 3) to explore proatherogenic effects of OPG on endothelial cells.
Results: OPG protein and mRNA expression was highly and significantly increased by IL-1β, insulin and glucose. OPG secretion to the supernatant was increased by IL-1β (4758 ± 727 vs. 88 ± 33 pg/mL, p=0.001) and PDGF (451 ± 151 vs. 88 ± 33 pg/mL, p=0.009). Glucose and insulin did not elevate OPG concentration in the supernatant. Endothelial cells stimulated with OPG significantly increased the release of IL-6 to the supernatant (247 ± 60 vs. 148 ± 30, p=0.008) and IL-8 was also increased by OPG (1444 ± 70 vs. 1538 ± 28, p=0.09).
Conclusion: Endothelial cells are a source of OPG in circulation and IL-1β, glucose and insulin stimulate its expression.