For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
15
views
162
references
 Top references
cited by
29
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      550
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      The role of monocytosis and neutrophilia in atherosclerosis

      review-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

          Monocytosis and neutrophilia are frequent events in atherosclerosis. These phenomena arise from the increased proliferation of hematopoietic stem and multipotential progenitor cells (HSPCs) and HSPC mobilization from the bone marrow to other immune organs and circulation. High cholesterol and inflammatory signals promote HSPC proliferation and preferential differentiation to the myeloid precursors ( i.e., myelopoiesis) that than give rise to pro‐inflammatory immune cells. These cells accumulate in the plaques thereby enhancing vascular inflammation and contributing to further lesion progression. Studies in animal models of atherosclerosis showed that manipulation with HSPC proliferation and differentiation through the activation of LXR‐dependent mechanisms and restoration of cholesterol efflux may have a significant therapeutic potential.

          Related collections

          Most cited references162

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

          Dynamic NETosis is Carried Out by Live Neutrophils in Human and Mouse Bacterial Abscesses and During Severe Gram-Positive Infection

          Bryan G Yipp, Björn Petri, Davide Salina … (2012)
          Neutrophil extracellular traps (NETs) are released, as neutrophils die in vitro, in a process requiring hours, leaving a temporal gap for invasive microbes to exploit. Functional neutrophils undergoing NETosis have not been documented. During Gram-positive skin infections, we directly visualized live PMN in vivo rapidly releasing NETs, which prevented bacterial dissemination. NETosis occurred during crawling thereby casting large areas of NETs. NET-releasing PMN developed diffuse decondensed nuclei ultimately becoming devoid of DNA. Cells with abnormal nuclei displayed unusual crawling behavior highlighted by erratic pseudopods and hyperpolarization consistent with the nucleus being a fulcrum for crawling. A combined requirement of Tlr2 and complement mediated opsonization tightly regulated NET release. Additionally live human PMN developed decondensed nuclei and formed NETS in vivo and intact anuclear neutrophils were abundant in Gram-positive human abscesses. Therefore early in infection, non-cell death NETosis occurs in vivo during Gram-positive infection in mice and humans.
          Article 0 comments Cited 454 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Myocardial infarction accelerates atherosclerosis

            Partha Dutta, Gabriel Courties, Ying Wei … (2012)
            SUMMARY During progression of atherosclerosis, myeloid cells destabilize lipid-rich plaque in the arterial wall and cause its rupture, thus triggering myocardial infarction and stroke. Survivors of acute coronary syndromes have a high risk of recurrent events for unknown reasons. Here we show that the systemic response to ischemic injury aggravates chronic atherosclerosis. After myocardial infarction or stroke, apoE−/− mice developed larger atherosclerotic lesions with a more advanced morphology. This disease acceleration persisted over many weeks and was associated with markedly increased monocyte recruitment. When seeking the source of surplus monocytes in plaque, we found that myocardial infarction liberated hematopoietic stem and progenitor cells from bone marrow niches via sympathetic nervous system signaling. The progenitors then seeded the spleen yielding a sustained boost in monocyte production. These observations provide new mechanistic insight into atherogenesis and provide a novel therapeutic opportunity to mitigate disease progression.
            Article 0 comments Cited 343 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              CXCR2 and CXCR4 antagonistically regulate neutrophil trafficking from murine bone marrow.

              Kyle Eash, Adam Greenbaum, Priya Gopalan … (2010)
              Neutrophils are a major component of the innate immune response. Their homeostasis is maintained, in part, by the regulated release of neutrophils from the bone marrow. Constitutive expression of the chemokine CXCL12 by bone marrow stromal cells provides a key retention signal for neutrophils in the bone marrow through activation of its receptor, CXCR4. Attenuation of CXCR4 signaling leads to entry of neutrophils into the circulation through unknown mechanisms. We investigated the role of CXCR2-binding ELR+ chemokines in neutrophil trafficking using mouse mixed bone marrow chimeras reconstituted with Cxcr2(-/-) and WT cells. In this context, neutrophils lacking CXCR2 were preferentially retained in the bone marrow, a phenotype resembling the congenital disorder myelokathexis, which is characterized by chronic neutropenia. Additionally, transient disruption of CXCR4 failed to mobilize Cxcr2(-/-) neutrophils. However, neutrophils lacking both CXCR2 and CXCR4 displayed constitutive mobilization, showing that CXCR4 plays a dominant role in neutrophil trafficking. With regard to CXCR2 ligands, bone marrow endothelial cells and osteoblasts constitutively expressed the ELR+ chemokines CXCL1 and CXCL2, and CXCL2 expression was induced in endothelial cells during G-CSF-induced neutrophil mobilization. Collectively, these data suggest that CXCR2 signaling is a second chemokine axis that interacts antagonistically with CXCR4 to regulate neutrophil release from the bone marrow.
              Article 0 comments Cited 282 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Alexander N. Orekhov:
                ORCID: http://orcid.org/0000-0002-6495-1628
                a.h.opexob@gmail.com
                Journal
                Journal ID (nlm-ta): J Cell Mol Med
                Journal ID (iso-abbrev): J. Cell. Mol. Med
                Journal ID (doi): 10.1111/(ISSN)1582-4934
                Journal ID (publisher-id): JCMM
                Title: Journal of Cellular and Molecular Medicine
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 1582-1838
                ISSN (Electronic): 1582-4934
                Publication date (Electronic): 24 January 2018
                Publication date (Print): March 2018
                Volume: 22
                Issue: 3 ( doiID: 10.1111/jcmm.2018.22.issue-3 )
                Pages: 1366-1382
                Affiliations
                [ 1 ] Department of Neurochemistry Division of Basic and Applied Neurobiology Serbsky Federal Medical Research Center of Psychiatry and Narcology Moscow Russia
                [ 2 ] Federal Scientific Clinical Center for Resuscitation and Rehabilitation Moscow Russia
                [ 3 ] Skolkovo Innovative Center Institute for Atherosclerosis Research Moscow Russia
                [ 4 ] Laboratory of Angiopathology Institute of General Pathology and Pathophysiology Russian Academy of Sciences Moscow Russia
                Author notes
                [*] [* ] Correspondence to: Alexander N. OREKHOV

                E‐mail: a.h.opexob@ 123456gmail.com

                Author information
                http://orcid.org/0000-0002-6495-1628
                Article
                Publisher ID: JCMM13462
                DOI: 10.1111/jcmm.13462
                PMC ID: 5824421
                PubMed ID: 29364567
                SO-VID: 242ab799-acaf-4106-9f7e-289db7abaa8e
                Copyright © © 2018 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
                License:

                This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 14 April 2017
                Date accepted : 09 October 2017
                Page count
                Figures: 2, Tables: 0, Pages: 17, Words: 14757
                Funding
                Funded by: Russian Science Foundation
                Award ID: 14‐15‐00112
                Categories
                Subject: Review
                Subject: Reviews
                Custom metadata
                source-schema-version-number 2.0
                component-id jcmm13462
                cover-date March 2018
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:version=5.3.2.2 mode:remove_FC converted:23.02.2018

                ScienceOpen disciplines: Molecular medicine
                Keywords: atherosclerosis,monocyte,neutrophil,chemokines,inflammation,atherosclerotic plaque
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: atherosclerosis, monocyte, neutrophil, chemokines, inflammation, atherosclerotic plaque

                Comments

                Comment on this article

                scite_

                Similar content550

                See all similar

                Cited by26

                See all cited by

                Most referenced authors3,613

                See all reference authors