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Fractalkine (CX3CL1) and Its Chemoattractant and Adhesion Molecule Properties in Health and Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 June 2024 | Viewed by 3106

Special Issue Editor

Prof. Dr. Dariusz Szukiewicz

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Guest Editor
Department of Biophysics, Physiology and Pathophysiology, Faculty of Health Sciences, Medical University of Warsaw, Chalubinskiego 5 (4th Floor), 02-004 Warsaw, Poland
Interests: inflammation; cytokine network; sirtuins; endothelial signaling; human placenta; stem cells; pathophysiology of diabetes
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Fractalkine (FKN), also known as CX3CL1, is the only member of the chemokine family containing a three amino acid motif between the two cysteines (C-X-X-X-C) and a mucin-like domain. This chemokine is made up of 373 amino acids and is synthesized as a transmembrane molecule. Moreover, after cleavage by the TNFα-converting enzyme ADAM17, FKN can exist in a soluble form. Such peculiar structural characteristics of fractalkine go hand in hand with its unique functional properties, because FKN combines the features of a chemoattractant and an adhesion molecule. Both of these functions require the presence of a specific and sole FKN receptor, CX3C motif chemokine receptor 1 (CX3CR1), also known as G-protein coupled receptor 13 (GPR13). Considering that CX3CR1 expression was demonstrated on many different cells, including but not limited to monocytes, microglia and macrophages, dendritic cells, T cells, natural killer (NK) cells, vascular endothelial cells, smooth and skeletal muscle cells, neurons, hepatocytes, adipocytes, and endometrial cells, FKN signaling may be crucial in health and disease. FKN-CX3CR1 signaling exerts distinct functions in different tissue compartments, and may be involved in a wide spectrum of biological phenomena such as cell adhesion and chemotaxis, immune response, inflammation, apoptosis, implantation, angiogenesis, atherosclerosis, formation of endometriotic foci, neurotoxicity, or carcinogenesis.

This Special Issue is dedicated to all aspects of FKN signaling, including both physiological and pathologic conditions. It may be extremely interesting to present the reasons for recognizing the FKN-CX3CR1 signaling pathway as the main therapeutic target in a given disease.

When considering your submission, please keep in mind that IJMS is a journal of molecular science. However, submissions of clinical studies that include biomolecular experiments or pathological research with case sample data are welcome.

Prof. Dr. Dariusz Szukiewicz
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

  • fractalkine
  • transmembrane fractalkine
  • soluble fractalkine
  • fractalkine receptor
  • CX3CL1-CX3CR1 signaling
  • inflammation
  • chemokine
  • cell adhesion
  • chemotaxis
  • immune response
  • angiogenesis
  • implantation
  • atherosclerosis
  • carcinogenesis

Published Papers (3 papers)

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Research

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20 pages, 7469 KiB  
Article
Effects of Cerebrospinal Fluids from Alzheimer and Non-Alzheimer Patients on Neurons–Astrocytes–Microglia Co-Culture
by Matilda Iemmolo, Giulia Bivona, Tommaso Piccoli, Aldo Nicosia, Gabriella Schiera, Carlo Maria Di Liegro, Fabrizio Di Pietra and Giulio Ghersi
Int. J. Mol. Sci. 2024, 25(5), 2510; https://doi.org/10.3390/ijms25052510 - 21 Feb 2024
Viewed by 770
Abstract
Alzheimer’s disease (AD) is the most common form of dementia, characterized by the accumulation of β-amyloid plaques, tau tangles, neuroinflammation, and synaptic/neuronal loss, the latter being the strongest correlating factor with memory and cognitive impairment. Through an in vitro study on a neurons–astrocytes–microglia [...] Read more.
Alzheimer’s disease (AD) is the most common form of dementia, characterized by the accumulation of β-amyloid plaques, tau tangles, neuroinflammation, and synaptic/neuronal loss, the latter being the strongest correlating factor with memory and cognitive impairment. Through an in vitro study on a neurons–astrocytes–microglia (NAM) co-culture system, we analyzed the effects of cerebrospinal fluid (CSF) samples from AD and non-AD patients (other neurodegenerative pathologies). Treatment with CSF from AD patients showed a loss of neurofilaments and spheroids, suggesting the presence of elements including CX3CL1 (soluble form), destabilizing the neurofilaments, cellular adhesion processes, and intercellular contacts. The NAM co-cultures were analyzed in immunofluorescence assays for several markers related to AD, such as through zymography, where the expression of proteolytic enzymes was quantified both in cell extracts and the co-cultures’ conditioned medium (CM). Through qRT-PCR assays, several genes involved in the formation of β-amyloid plaque, in phosphorylation of tau, and in inflammation pathways and MMP expression were investigated. Full article
(This article belongs to the Special Issue Fractalkine (CX3CL1) and Its Chemoattractant and Adhesion Molecule Properties in Health and Disease)
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Review

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17 pages, 1133 KiB  
Review
Alterations in CX3CL1 Levels and Its Role in Viral Pathogenesis
by Chunmei Zhang, Yusi Zhang, Ran Zhuang, Kun Yang, Lihua Chen, Boquan Jin, Ying Ma, Yun Zhang and Kang Tang
Int. J. Mol. Sci. 2024, 25(8), 4451; https://doi.org/10.3390/ijms25084451 - 18 Apr 2024
Viewed by 638
Abstract
CX3CL1, also named fractalkine or neurotactin, is the only known member of the CX3C chemokine family that can chemoattract several immune cells. CX3CL1 exists in both membrane-anchored and soluble forms, with each mediating distinct biological activities. CX3CL1 signals are transmitted through its unique [...] Read more.
CX3CL1, also named fractalkine or neurotactin, is the only known member of the CX3C chemokine family that can chemoattract several immune cells. CX3CL1 exists in both membrane-anchored and soluble forms, with each mediating distinct biological activities. CX3CL1 signals are transmitted through its unique receptor, CX3CR1, primarily expressed in the microglia of the central nervous system (CNS). In the CNS, CX3CL1 acts as a regulator of microglia activation in response to brain disorders or inflammation. Recently, there has been a growing interest in the role of CX3CL1 in regulating cell adhesion, chemotaxis, and host immune response in viral infection. Here, we provide a comprehensive review of the changes and function of CX3CL1 in various viral infections, such as human immunodeficiency virus (HIV), SARS-CoV-2, influenza virus, and cytomegalovirus (CMV) infection, to highlight the emerging roles of CX3CL1 in viral infection and associated diseases. Full article
(This article belongs to the Special Issue Fractalkine (CX3CL1) and Its Chemoattractant and Adhesion Molecule Properties in Health and Disease)
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17 pages, 882 KiB  
Review
Chemokine Fractalkine and Non-Obstructive Coronary Artery Disease—Is There a Link?
by Aleksandra Stangret, Karol Artur Sadowski, Konrad Jabłoński, Janusz Kochman, Grzegorz Opolski, Marcin Grabowski and Mariusz Tomaniak
Int. J. Mol. Sci. 2024, 25(7), 3885; https://doi.org/10.3390/ijms25073885 - 30 Mar 2024
Viewed by 1206
Abstract
Non-obstructive coronary artery disease (NO-CAD) constitutes a heterogeneous group of conditions collectively characterized by less than 50% narrowing in at least one major coronary artery with a fractional flow reserve (FFR) of ≤0.80 observed in coronary angiography. The pathogenesis and progression of NO-CAD [...] Read more.
Non-obstructive coronary artery disease (NO-CAD) constitutes a heterogeneous group of conditions collectively characterized by less than 50% narrowing in at least one major coronary artery with a fractional flow reserve (FFR) of ≤0.80 observed in coronary angiography. The pathogenesis and progression of NO-CAD are still not fully understood, however, inflammatory processes, particularly atherosclerosis and microvascular dysfunction are known to play a major role in it. Chemokine fractalkine (FKN/CX3CL1) is inherently linked to these processes. FKN/CX3CL1 functions predominantly as a chemoattractant for immune cells, facilitating their transmigration through the vessel wall and inhibiting their apoptosis. Its concentrations correlate positively with major cardiovascular risk factors. Moreover, promising preliminary results have shown that FKN/CX3CL1 receptor inhibitor (KAND567) administered in the population of patients with ST-elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI), inhibits the adverse reaction of the immune system that causes hyperinflammation. Whereas the link between FKN/CX3CL1 and NO-CAD appears evident, further studies are necessary to unveil this complex relationship. In this review, we critically overview the current data on FKN/CX3CL1 in the context of NO-CAD and present the novel clinical implications of the unique structure and function of FKN/CX3CL1 as a compound which distinctively contributes to the pathomechanism of this condition. Full article
(This article belongs to the Special Issue Fractalkine (CX3CL1) and Its Chemoattractant and Adhesion Molecule Properties in Health and Disease)
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