ijms-logo

Journal Browser

Journal Browser

Molecular Mechanisms of C-Reactive Protein

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 20 January 2025 | Viewed by 1780

Special Issue Editor


E-Mail Website
Guest Editor
1. Center for Advanced Medical and Pharmaceutical Research (CCAMF), George Emil Palade University of Medicine, Pharmacy, Science and Technology of Targu Mures, 540142 Targu Mures, Romania
2. Department of Life Sciences, Manchester Metropolitan University, Manchester M15 6BH, UK
Interests: C-reactive protein

Special Issue Information

Dear Colleagues,

The aim of this series is to provide an understanding of the complex cell and molecular mechanisms through which monomeric C-reactive protein (mCRP) induces responses in host tissues and cells, driving various pathological conditions. In this group of publications, the receptor-mediated activation of signaling pathways linked to inflammation, angiogenesis, and other aberrant responses will be evaluated. The link between mCRP and the development as well as progression of both acute and chronic diseases, such as atherosclerosis, Alzheimer’s disease, diabetes, and diabetic complications, can be considered within this series.

This Special Issue of the International Journal of Molecular Sciences on “Molecular Mechanisms of C-Reactive Protein”, supervised by Prof. Dr. Mark Slevin (Manchester Metropolitan University; George Emil Palade University of Medicine, Pharmacy, Science and Technology of Targu Mures) and assisted by Dr. Ylenia Pastorello (George Emil Palade University of Medicine, Pharmacy, Science and Technology of Targu Mures), aims at providing cutting-edge knowledge on every aspect of C-reactive protein.

Prof. Dr. Mark Slevin
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • C-reactive protein
  • cell signalling
  • inflammation
  • pathological processes

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

14 pages, 3305 KiB  
Article
mCRP-Induced Focal Adhesion Kinase-Dependent Monocyte Aggregation and M1 Polarization, Which Was Partially Blocked by the C10M Inhibitor
by Ylenia Pastorello, Doina Manu, Xenia Sawkulycz, Vittorio Caprio, Claudia Banescu, Minodora Dobreanu, Lawrence Potempa, Mario Di Napoli and Mark Slevin
Int. J. Mol. Sci. 2024, 25(6), 3097; https://doi.org/10.3390/ijms25063097 - 7 Mar 2024
Cited by 1 | Viewed by 1233
Abstract
Monomeric C-reactive protein (mCRP) has recently been implicated in the abnormal vascular activation associated with development of atherosclerosis, but it may act more specifically through mechanisms perpetuating damaged vessel inflammation and subsequent aggregation and internalization of resident macrophages. Whilst the direct effects of [...] Read more.
Monomeric C-reactive protein (mCRP) has recently been implicated in the abnormal vascular activation associated with development of atherosclerosis, but it may act more specifically through mechanisms perpetuating damaged vessel inflammation and subsequent aggregation and internalization of resident macrophages. Whilst the direct effects of mCRP on endothelial cells have been characterized, the interaction with blood monocytes has, to our knowledge, not been fully defined. Here we showed that mCRP caused a strong aggregation of both U937 cell line and primary peripheral blood monocytes (PBMs) obtained from healthy donors. Moreover, this increase in clustering was dependent on focal adhesion kinase (FAK) activation (blocked by a specific inhibitor), as was the concomitant adhesive attachment to the plate, which was suggestive of macrophage differentiation. Confocal microscopy confirmed the increased expression and nuclear localization of p-FAK, and cell surface marker expression associated with M1 macrophage polarization (CD11b, CD14, and CD80, as well as iNOS) in the presence of mCRP. Inclusion of a specific CRP dissociation/mCRP inhibitor (C10M) effectively inhibited PBMs clustering, as well as abrogating p-FAK expression, and partially reduced the expression of markers associated with M1 macrophage differentiation. mCRP also increased the secretion of pro-inflammatory cytokines Interleukin-8 (IL-8) and Interleukin-1β (IL-1β), without notably affecting MAP kinase signaling pathways; inclusion of C10M did not perturb or modify these effects. In conclusion, mCRP modulates PBMs through a mechanism that involves FAK and results in cell clustering and adhesion concomitant with changes consistent with M1 phenotypical polarization. C10M has potential therapeutic utility in blocking the primary interaction of mCRP with the cells—for example, by protecting against monocyte accumulation and residence at damaged vessels that may be predisposed to plaque development and atherosclerosis. Full article
(This article belongs to the Special Issue Molecular Mechanisms of C-Reactive Protein)
Show Figures

Figure 1

Back to TopTop