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CRP enhances soluble LOX-1 release from macrophages by activating TNF-α converting enzyme. | LitMetric

CRP enhances soluble LOX-1 release from macrophages by activating TNF-α converting enzyme.

J Lipid Res

The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health, Qilu Hospital of Shandong University, Jinan, Shandong 250012, China.

Published: May 2011

AI Article Synopsis

  • High levels of soluble lectin-like oxidized low-density lipoprotein receptor-1 (sLOX-1) are linked to atherosclerosis, and the study investigates how C-reactive protein (CRP) affects sLOX-1 release from macrophages.
  • The research found that CRP increases sLOX-1 release in a dose-dependent manner through mechanisms involving p47(phox) phosphorylation, reactive oxygen species (ROS) production, and activation of tumor necrosis factor-α converting enzyme (TACE).
  • In both lab-made macrophages and those from patients with acute coronary syndrome, inhibiting certain pathways reduced the CRP-induced sLOX-1 release, suggesting that CRP plays a significant

Article Abstract

Circulating levels of soluble lectin-like oxidized low-density lipoprotein receptor-1 (sLOX-1) play an important role in the development and progression of atherosclerosis. We hypothesized that the inflammatory marker C-reactive protein (CRP) might stimulate sLOX-1 release by activating tumor necrosis factor-α converting enzyme (TACE). Macrophages differentiated from THP-1 cells were stimulated with TNF-α and further treated with CRP in the absence or presence of specific inhibitors or small interfering RNA (siRNA). Our results showed that CRP increased sLOX-1 release from activated macrophages in a dose-dependent manner and that these effects were regulated by Fc γ receptor II (FcγRII)-mediated p47(phox) phosphorylation, reactive oxygen species (ROS) production, and TACE activation. CRP also enhanced sLOX-1 release from macrophages derived from peripheral blood mononuclear cells (PBMC) of patients with acute coronary syndrome (ACS). Pretreatment with antibody against FcγRII or with CD32 siRNA, p47(phox) siRNA, apocynin, N-acetylcysteine, tumor necrosis factor-α protease inhibitor 1 (TAPI-1) or TACE siRNA attenuated sLOX-1 release induced by CRP. CRP also elevated serum sLOX-1 levels in a rabbit model of atherosclerosis. Thus, CRP might stimulate sLOX-1 release, and the underlying mechanisms possibly involved FcγRII-mediated p47(phox) phosphorylation, ROS production, and TACE activation.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3072294PMC
http://dx.doi.org/10.1194/jlr.M015156DOI Listing

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