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Regulation of Cytokine Signaling in Health and Disease

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A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Biological Factors".

Deadline for manuscript submissions: closed (29 February 2024) | Viewed by 7764

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Special Issue Editor

Prof. Dr. Alister C. Ward

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Guest Editor

School of Medicine, Centre of Molecular and Medical Research, Deakin University, Waurn Ponds, VIC 3216, Australia
Interests: cytokines; cell signaling; JAK-STAT pathway; SOCS; hematopoiesis; leukocytes lymphocytes; leukemia; lymphoma
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to invite researchers to contribute to the following Special Issue.

Cytokine receptors are expressed on the surfaces of responsive cells, notably the blood and immune cells, in which they mediate important cell–cell communications. This results in the activation of the intracellular signaling pathways that drive a multitude of critical cell processes, such as differentiation, proliferation, activation and survival. Such signaling is essential for the normal development and function of many cell lineages, and its perturbation can lead to a variety of pathological states. Consequently, cytokine receptor signaling is controlled on multiple levels. This Special Issue will focus on the regulation of cytokine receptor signaling and its importance in the contexts of health and disease.

This Special Issue, entitled ‘Regulation of Cytokine Signaling in Health and Disease’, aims to explore different facets of cytokine receptor signaling regulation and the ways in which they facilitate normal cell development and function and/or how the perturbation of this regulation leads to disease.

We welcome authors to submit original research articles and reviews to this Special Issue. Paper topics can include any aspect of cytokine receptor signaling regulation, from clinical studies through to research using cell and animal models.

We look forward to receiving your contributions.

Prof. Dr. Alister C. Ward
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. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

cytokine receptor
cell signaling
development
disease
cancer

Published Papers (5 papers)

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Research

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13 pages, 2465 KiB

Open AccessArticle

C-C Motif Chemokine Ligand 2 Enhances Macrophage Chemotaxis, Osteogenesis, and Angiogenesis during the Inflammatory Phase of Bone Regeneration

by Issei Shinohara, Masanori Tsubosaka, Masakazu Toya, Max L. Lee, Junichi Kushioka, Masatoshi Murayama, Qi Gao, Xueping Li, Ning Zhang, Simon Kwoon-Ho Chow, Tomoyuki Matsumoto, Ryosuke Kuroda and Stuart B. Goodman

Biomolecules 2023, 13(11), 1665; https://doi.org/10.3390/biom13111665 - 18 Nov 2023

Cited by 3 | Viewed by 1141

Abstract

Local cell therapy has recently gained attention for the treatment of joint diseases and fractures. Mesenchymal stem cells (MSCs) are not only involved in osteogenesis and angiogenesis, but they also have immunomodulatory functions, such as inducing macrophage migration during bone regeneration via macrophage crosstalk. C-C motif chemokine ligand 2 (CCL2), a known inflammatory mediator, is associated with the migration of macrophages during inflammation. This study examined the utility of CCL2 as a therapeutic target for local cell therapy. Using lentiviral vectors for rabbit MSCs, genetically modified CCL2 overexpressing MSCs were generated. Osteogenic differentiation assays were performed using MSCs with or without macrophages in co-culture, and cell migration assays were also performed. Additionally, co-cultures were performed with endothelial cells (ECs), and angiogenesis was evaluated using a tube formation assay. Overexpression of CCL2 did not affect bone formation under monoculture conditions but promoted chemotaxis and osteogenesis when co-cultured with macrophages. Furthermore, CCL2-overexpression promoted tube formation in co-culture with ECs. These results suggest that CCL2 induces macrophage chemotaxis and osteogenesis by promoting crosstalk between MSCs and macrophages; CCL2 also stimulates ECs to induce angiogenesis. These findings indicate that CCL2 may be a useful therapeutic target for local cell therapy in areas of bone loss. Full article

(This article belongs to the Special Issue Regulation of Cytokine Signaling in Health and Disease)

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11 pages, 1908 KiB

Open AccessArticle

Role of Cytokine-Inducible SH2 Domain-Containing (CISH) Protein in the Regulation of Erythropoiesis

by Saeed Maymand, Asha L. Lakkavaram, Wasan Naser, Parisa Rasighaemi, Daniel Dlugolenski, Clifford Liongue, John Stambas, Tania F. de Koning-Ward and Alister C. Ward

Biomolecules 2023, 13(10), 1510; https://doi.org/10.3390/biom13101510 - 12 Oct 2023

Cited by 1 | Viewed by 977

Abstract

The cytokine-inducible SH2 domain-containing (CISH) protein was the first member of the suppressor of cytokine signaling (SOCS) family of negative feedback regulators discovered, being identified in vitro as an inducible inhibitor of erythropoietin (EPO) signaling. However, understanding of the physiological role played by CISH in erythropoiesis has remained limited. To directly assess the function of CISH in this context, mice deficient in CISH were characterized with respect to developmental, steady-state, and EPO-induced erythropoiesis. CISH was strongly expressed in the fetal liver, but CISH knockout (KO) mice showed only minor disruption of primitive erythropoiesis. However, adults exhibited mild macrocytic anemia coincident with subtle perturbation particularly of bone marrow erythropoiesis, with EPO-induced erythropoiesis blunted in the bone marrow of KO mice but enhanced in the spleen. Cish was expressed basally in the bone marrow with induction following EPO stimulation in bone marrow and spleen. Overall, this study indicates that CISH participates in the control of both basal and EPO-induced erythropoiesis in vivo. Full article

(This article belongs to the Special Issue Regulation of Cytokine Signaling in Health and Disease)

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15 pages, 6689 KiB

Open AccessEditor’s ChoiceArticle

The Effects of an Osteoarthritic Joint Environment on ACL Damage and Degeneration: A Yucatan Miniature Pig Model

by Elias Schwartz, Kenny Chang, Changqi Sun, Fei Zhang, Guoxuan Peng, Brett Owens and Lei Wei

Biomolecules 2023, 13(9), 1416; https://doi.org/10.3390/biom13091416 - 20 Sep 2023

Viewed by 914

Abstract

Posttraumatic osteoarthritis (PTOA) arises secondary to joint injuries and is characteristically driven by inflammatory mediators. PTOA is often studied in the setting of ACL tears. However, a wide range of other injuries also lead to PTOA pathogenesis. The purpose of this study was to characterize the morphological changes in the uninjured ACL in a PTOA inflammatory environment. We retrospectively reviewed 14 ACLs from 13 Yucatan minipigs, 7 of which had undergone our modified intra-articular drilling (mIAD) procedure, which induced PTOA through inflammatory mediators. Seven ACLs were harvested from mIAD minipigs (PTOA) and seven ACLs from control minipigs with no cartilage degeneration (non-PTOA). ACL degeneration was evaluated using histological scoring systems. IL-1β, NF-κB, and TNF-α mRNA expression in the synovium was measured using qRT-PCR. PTOA minipigs demonstrated significant ACL degeneration, marked by a disorganized extracellular matrix, increased vascularity, and changes in cellular shape, density, and alignment. Furthermore, IL-1β, NF-κB, and TNF-α expression was elevated in the synovium of PTOA minipigs. These findings demonstrate the potential for ACL degeneration in a PTOA environment and emphasize the need for anti-inflammatory disease-modifying therapies following joint injury. Full article

(This article belongs to the Special Issue Regulation of Cytokine Signaling in Health and Disease)

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14 pages, 3149 KiB

Open AccessArticle

Force-Regulated Calcium Signaling of Lymphoid Cell RPMI 8226 Mediated by Integrin α₄β₇/MAdCAM-1 in Flow

by Dongshan Sun, Zhiqing Luo, Ying Kong, Ruiting Huang and Quhuan Li

Biomolecules 2023, 13(4), 587; https://doi.org/10.3390/biom13040587 - 24 Mar 2023

Cited by 1 | Viewed by 1508

Abstract

MAdCAM-1 binds to integrin α₄β₇, which mediates the rolling and arrest of circulating lymphocytes upon the vascular endothelia during lymphocytic homing. The calcium response by adhered lymphocytes is a critical event for lymphocyte activation and subsequent arrest and migration under flow. However, whether the interaction of integrin α₄β₇ /MAdCAM-1 can effectively trigger the calcium response of lymphocytes remains unclear, as well as whether the fluid force affects the calcium response. In this study, we explore the mechanical regulation of integrin α₄β₇-induced calcium signaling under flow. Flou-4 AM was used to examine the calcium response under real-time fluorescence microscopy when cells were firmly adhered to a parallel plate flow chamber. The interaction between integrin α₄β₇ and MAdCAM-1 was found to effectively trigger calcium signaling in firmly adhered RPMI 8226 cells. Meanwhile, increasing fluid shear stress accelerated the cytosolic calcium response and enhanced signaling intensity. Additionally, the calcium signaling of RPMI 8226 activated by integrin α₄β₇ originated from extracellular calcium influx instead of cytoplasmic calcium release, and the signaling transduction of integrin α₄β₇ was involved in Kindlin-3. These findings shed new light on the mechano-chemical mechanism of calcium signaling in RPMI 8226 cells induced by integrin α₄β_7. Full article

(This article belongs to the Special Issue Regulation of Cytokine Signaling in Health and Disease)

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Review

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19 pages, 1779 KiB

Open AccessEditor’s ChoiceReview

The Molecular and Genetic Mechanisms of Inherited Bone Marrow Failure Syndromes: The Role of Inflammatory Cytokines in Their Pathogenesis

by Nozomu Kawashima, Valentino Bezzerri and Seth J. Corey

Biomolecules 2023, 13(8), 1249; https://doi.org/10.3390/biom13081249 - 16 Aug 2023

Cited by 1 | Viewed by 2619

Abstract

Inherited bone marrow failure syndromes (IBMFSs) include Fanconi anemia, Diamond–Blackfan anemia, Shwachman–Diamond syndrome, dyskeratosis congenita, severe congenital neutropenia, and other rare entities such as GATA2 deficiency and SAMD9/9L mutations. The IBMFS monogenic disorders were first recognized by their phenotype. Exome sequencing has validated their classification, with clusters of gene mutations affecting DNA damage response (Fanconi anemia), ribosome structure (Diamond–Blackfan anemia), ribosome assembly (Shwachman–Diamond syndrome), or telomere maintenance/stability (dyskeratosis congenita). The pathogenetic mechanisms of IBMFSs remain to be characterized fully, but an overarching hypothesis states that different stresses elicit TP53-dependent growth arrest and apoptosis of hematopoietic stem, progenitor, and precursor cells. Here, we review the IBMFSs and propose a role for pro-inflammatory cytokines, such as TGF-β, IL-1β, and IFN-α, in mediating the cytopenias. We suggest a pathogenic role for cytokines in the transformation to myeloid neoplasia and hypothesize a role for anti-inflammatory therapies. Full article

(This article belongs to the Special Issue Regulation of Cytokine Signaling in Health and Disease)

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