For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
24
views
25
references
 Top references
cited by
11
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      160
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      A significant correlation between C - reactive protein levels in blood monocytes derived macrophages versus content in carotid atherosclerotic lesions

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          Atherosclerosis is a complex disease involving different cell types, including macrophages that play a major role in the inflammatory events occurring in atherogenesis. C-Reactive Protein (CRP) is a sensitive systemic marker of inflammation and was identified as a biomarker of cardiovascular diseases. Histological studies demonstrate CRP presence in human atherosclerotic lesions, and we have previously shown that macrophages express CRP mRNA. CRP could be locally secreted in the atherosclerotic lesion by arterial macrophages and local regulation of CRP could affect its pro-atherogenic effects. Moreover, human blood derived macrophages (HMDM) expression of CRP could reflect atherosclerotic lesion secretion of CRP.

          Methods

          Ten type 2 diabetic patients and ten non-diabetic patients scheduled to undergo carotid endarterectomy were enrolled in this study, and their blood samples were used for serum CRP, lipid determination, and for preparation of HMDM further analyzed for their CRP mRNA expression and CRP content. Carotid lesions obtained from the patients were analyzed for their CRP and interleukin 6 (IL-6) content by immunohistochemistry.

          Results

          Lesions from diabetic patients showed substantially higher CRP levels by 62% (p = 0.05) than lesions from non diabetic patients, and CRP staining that co-localized with arterial macrophages. CRP carotid lesion levels positively correlated with CRP mRNA expression (r 2 = 0.661) and with CRP content (r 2 = 0.611) in the patient’s HMDM.

          Conclusions

          Diabetes up-regulated carotid plaques CRP levels and CRP measurements in HMDM could reflect atherosclerotic lesion macrophages secretion of CRP. Understanding the regulation of locally produced macrophage CRP in the arterial wall during atherogenesis could be of major importance in identifying the underlying mechanisms of inflammatory response pathways during atherogenesis.

          Related collections

          Most cited references25

          • Record: found
          • Abstract: found
          • Article: not found

          Monocyte and macrophage dynamics during atherogenesis.

          Klaus Ley, Yury Miller, Catherine C. Hedrick (2011)
          Vascular inflammation is associated with and in large part driven by changes in the leukocyte compartment of the vessel wall. Here, we focus on monocyte influx during atherosclerosis, the most common form of vascular inflammation. Although the arterial wall contains a large number of resident macrophages and some resident dendritic cells, atherosclerosis drives a rapid influx of inflammatory monocytes (Ly-6C(+) in mice) and other monocytes (Ly-6C(-) in mice, also known as patrolling monocytes). Once in the vessel wall, Ly-6C(+) monocytes differentiate to a phenotype consistent with inflammatory macrophages and inflammatory dendritic cells. The phenotype of these cells is modulated by lipid uptake, Toll-like receptor ligands, hematopoietic growth factors, cytokines, and chemokines. In addition to newly recruited macrophages, it is likely that resident macrophages also change their phenotype. Monocyte-derived inflammatory macrophages have a short half-life. After undergoing apoptosis, they may be taken up by surrounding macrophages or, if the phagocytic capacity is overwhelmed, can undergo secondary necrosis, a key event in forming the necrotic core of atherosclerotic lesions. In this review, we discuss these and other processes associated with monocytic cell dynamics in the vascular wall and their role in the initiation and progression of atherosclerosis.
          Article 0 comments Cited 172 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Mineralocorticoid receptor blocker increases angiotensin-converting enzyme 2 activity in congestive heart failure patients.

            A Gamliel-Lazarovich, Shadi Hamoud, Elsa Pavlotzky … (2005)
            Aldosterone plays an important role in the pathophysiology of congestive heart failure (CHF), and spironolactone improves cardiovascular function and survival rates in patients with CHF. We hypothesized that the mineralocorticoid receptor blockade (MRB) exerted its beneficial effects by reducing oxidative stress and changing the balance between the counter-acting enzymes angiotensin-converting enzyme (ACE) and ACE2. Monocyte-derived macrophages were obtained from 10 patients with CHF before and after 1 month of treatment with spironolactone (25 mg/d). Spironolactone therapy significantly (P<0.005) reduced oxidative stress, as expressed by reduced lipid peroxide content, superoxide ion release, and low-density lipoprotein oxidation by 28%, 53%, and 70%, respectively. Although spironolactone significantly (P<0.01) reduced macrophage ACE activity by 47% and mRNA expression by 53%, ACE2 activity and mRNA expression increased by 300% and 654%, respectively. In mice treated for 2 weeks with eplerenone (200 mg.kg(-1).d(-1)), cardiac ACE2 activity significantly (P<0.05) increased by 2-fold and was paralleled by increased ACE2 activity in macrophages. The mechanism of aldosterone antagonist action was studied in mouse peritoneal macrophages (MPMs) in vitro. Although ACE activity and mRNA were significantly increased by 250 nmol/L aldosterone, ACE2 was significantly reduced. Cotreatment with eplerenone (2 micromol/L) attenuated these effects. In MPM obtained from p47 knockout mice, where NADPH oxidase is inactive, as well as in control MPMs treated with NADPH oxidase inhibitor, aldosterone did not increase ACE or decrease ACE2. MRB reduced oxidative stress, decreased ACE activity, and increased ACE2 activity, suggesting a protective role for MRB by possibly increasing generation of angiotensin (1-7) and decreasing formation of angiotensin II. These effects are mediated, at least in part, by NADPH oxidase.
            Article 0 comments Cited 95 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Proinflammatory cytokines in CRP baseline regulation.

              Aron C. Eklund (2008)
              Low-grade inflammation, a minor elevation in the baseline concentration of inflammatory markers such as C-reactive protein (CRP), is nowadays recognized as an important underlying condition in many common diseases. Concentrations of CRP under 10 mg/1 are called low-grade inflammation and values above that are considered as clinically significant inflammatory states. Epidemiological studies have revealed demographic and socioeconomic factors that associate with CRP concentration; these include age, sex, birth weight, ethnicity, socioeconomic status, body mass index (BMI), fiber consumption, alcohol intake, and dietary fatty acids. At the molecular level, production of CRP is induced by proinflammatory cytokines IL-1, IL-6, and IL-17 in the liver, although extra hepatic production most likely contributes to systemic concentrations. The cytokines are produced in response to, for example, steroid hormones, thrombin, C5a, bradykinin, other cytokines, UV-light, neuropeptides and bacterial components, such as lipopolysaccharide. Cytokines exert their biological effects on CRP by signaling through their receptors on hepatic cells and activating different kinases and phosphatases leading to translocation of various transcription factors on CRP gene promoter and production of CRP protein. Genetic polymorphisms in the interleukin genes as well as in CRP gene have been associated with minor elevation in CRP. As minor elevation in CRP is associated with both inflammatory and noninflammatory conditions, it should be noticed that the elevation might just reflect distressed or injured cells homeostasis maintenance in everyday life, rather than inflammation with classical symptoms of redness, swelling, heat, and pain.
              Article 0 comments Cited 67 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Marielle Kaplan
                Shadi Hamoud
                Yevgeny Tendler
                Edna Meilin
                Aviva Lazarovitch
                Samy Nitecki
                Tony Hayek
                Journal
                Journal ID (nlm-ta): J Inflamm (Lond)
                Journal ID (iso-abbrev): J Inflamm (Lond)
                Title: Journal of Inflammation (London, England)
                Publisher: BioMed Central
                ISSN (Electronic): 1476-9255
                Publication date Collection: 2014
                Publication date (Electronic): 3 March 2014
                Volume: 11
                Page: 7
                Affiliations
                [1 ]Laboratory of Clinical Biochemistry, Rambam Health Care Campus, Haifa, Israel
                [2 ]Department of Internal Medicine E, Rambam Health Care Campus, Haifa, Israel
                [3 ]Lipid Research Laboratory, The Ruth and Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel
                [4 ]Department of Vascular Surgery, Rambam Health Care Campus, Haifa, Israel
                Article
                Publisher ID: 1476-9255-11-7
                DOI: 10.1186/1476-9255-11-7
                PMC ID: 3944991
                PubMed ID: 24588988
                SO-VID: 9a99d195-489a-483a-8077-684821b4bcec
                Copyright © Copyright © 2014 Kaplan et al.; licensee BioMed Central Ltd.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited.

                History
                Date received : 6 April 2013
                Date accepted : 17 February 2014
                Categories
                Subject: Research

                ScienceOpen disciplines: Immunology
                Keywords: c-reactive protein,atherosclerosis,macrophages,inflammation
                Data availability:
                ScienceOpen disciplines: Immunology
                Keywords: c-reactive protein, atherosclerosis, macrophages, inflammation

                Comments

                Comment on this article

                scite_

                Similar content160

                See all similar

                Cited by9

                See all cited by

                Most referenced authors711

                See all reference authors