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Prof. Dr. Mark Slevin

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1. Department of Anatomy, George Emil Palade University of Medicine, Pharmacy, Science and Technology of Targu Mures, 540142 Targu Mures, Romania
2. The School of Life Sciences, Manchester Metropolitan University, Manchester M1 5QA, UK
Interests: C-reactive protein

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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

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Keywords

C-reactive protein
cell signalling
inflammation
pathological processes

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14 pages, 3305 KiB

Open AccessArticle

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 - 07 Mar 2024

Viewed by 559

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 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)

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