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Editorial Board Members' Collection Series: Cell Signaling in Health and Disease

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A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cell Biology".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 7933

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Special Issue Editors

Prof. Dr. Michael J. Bouchard

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Guest Editor

Department of Biochemistry & Molecular Biology, Drexel University College of Medicine, Philadelphia, PA 19129, USA
Interests: liver cancer; hepatocyte transformation; calcium signaling; apoptosis; cell proliferation; novel liver models; hepatitis B virology

Prof. Dr. Francesco Cappello

E-Mail Website
Guest Editor

Department of Biomedicine, Neuroscience and Advanced Diagnostics (BiND), University of Palermo, 90127 Palermo, Italy
Interests: cell differentiation; tissue homeostasis; organ remodeling; cell stress; chaperones; heat shock proteins; chaperonopathies; exosomes
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The pathogenesis of virtually all disease originates from an impairment of cell differentiation. This, in turn, determines the alteration of tissue homeostasis and defecting organ remodeling. Physicians and researchers need to have good knowledge about cell biology and morphology to investigate the molecular basis of disease and develop new therapeutical strategies.

We invite the submission of original research articles and reviews to this Special Issue focusing on the wide subject of “cell signaling” in health and disease, including discussions not only of adult life but also of pre-natal (embryo & fetus) and childhood ages. An impairment in cell signaling can cause transformation of a healthy tissue into a damaged organ at any point in a lifespan (including ageing) and in all anatomical districts, such as the heart, nervous system, liver, kidney, skeletal muscle, and many other viscera.

This Special Issue aims to offer to our readers novel knowledge about cell signaling in health and disease.

Research areas may include (but not limited to) the following topics:

Cell Biology
Genetics
Molecular Biology
Molecular Anatomy
Histology
Embryology
Pathophysiology
Pharmacology
Pathological Anatomy
Internal medicine

We look forward to receiving your contributions.

Prof. Dr. Michael J. Bouchard
Prof. Dr. Francesco Cappello
Guest Editors

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. Biology 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

disease pathophysiology
cell differentiation
tissue homeostasis
organ remodeling
cell biology
cell morphology
embryology
human anatomy
organogenesis
organ meiopragia

Published Papers (5 papers)

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Research

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18 pages, 5490 KiB

Open AccessArticle

NF-kB Regulation and the Chaperone System Mediate Restorative Effects of the Probiotic Lactobacillus fermentum LF31 in the Small Intestine and Cerebellum of Mice with Ethanol-Induced Damage

by Letizia Paladino, Francesca Rappa, Rosario Barone, Filippo Macaluso, Francesco Paolo Zummo, Sabrina David, Marta Anna Szychlinska, Fabio Bucchieri, Everly Conway de Macario, Alberto J. L. Macario, Francesco Cappello and Antonella Marino Gammazza

Biology 2023, 12(11), 1394; https://doi.org/10.3390/biology12111394 - 01 Nov 2023

Cited by 1 | Viewed by 1231

Abstract

Probiotics are live microorganisms that yield health benefits when consumed, generally by improving or restoring the intestinal flora (microbiota) as part of the muco-microbiotic layer of the bowel. In this work, mice were fed with ethanol alone or in combination with the probiotic Lactobacillus fermentum (L. fermentum) for 12 weeks. The modulation of the NF-κB signaling pathway with the induction of Hsp60, Hsp90, and IkB-α by the probiotic occurred in the jejunum. L. fermentum inhibited IL-6 expression and downregulated TNF-α transcription. NF-κB inactivation concurred with the restoration of the intestinal barrier, which had been damaged by ethanol, via the production of tight junction proteins, ameliorating the ethanol-induced intestinal permeability. The beneficial effect of the probiotic on the intestine was repeated for the cerebellum, in which downregulation of glial inflammation-related markers was observed in the probiotic-fed mice. The data show that L. fermentum exerted anti-inflammatory and cytoprotective effects in both the small intestine and the cerebellum, by suppressing ethanol-induced increased intestinal permeability and curbing neuroinflammation. The results also suggest that L. fermentum could be advantageous, along with the other available means, for treating intestinal diseases caused by stressors associated with inflammation and dysbiosis. Full article

(This article belongs to the Special Issue Editorial Board Members' Collection Series: Cell Signaling in Health and Disease)

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18 pages, 2853 KiB

Open AccessArticle

Bone Morphogenic Proteins and Their Antagonists in the Lower Airways of Stable COPD Patients

by Antonino Di Stefano, Umberto Rosani, Stefano Levra, Isabella Gnemmi, Paola Brun, Mauro Maniscalco, Silvestro Ennio D’Anna, Vitina Carriero, Francesca Bertolini and Fabio L. M. Ricciardolo

Biology 2023, 12(10), 1304; https://doi.org/10.3390/biology12101304 - 03 Oct 2023

Cited by 2 | Viewed by 1026

Abstract

Background: Bone morphogenic proteins (BMPs) and their antagonists are involved in the tissue development and homeostasis of various organs. Objective: To determine transcriptomic and protein expression of BMPs and their antagonists in stable COPD. Methods: We measured the expression and localization of BMPs and some relevant antagonists in bronchial biopsies of stable mild/moderate COPD (MCOPD) (n = 18), severe/very severe COPD (SCOPD) (n = 16), control smokers (CS) (n = 13), and control non-smokers (CNS) (n = 11), and in lung parenchyma of MCOPD (n = 9), CS (n = 11), and CNS (n = 9) using immunohistochemistry and transcriptome analysis, in vitro after the stimulation of the 16HBE cells. Results: In bronchial biopsies, BMP4 antagonists CRIM1 and chordin were increased in the bronchial epithelium and lamina propria of COPD patients. BMP4 expression was decreased in the bronchial epithelium of SCOPD and MCOPD compared to CNS. Lung transcriptomic data showed non-significant changes between groups. CRIM1 and chordin were significantly decreased in the alveolar macrophages and alveolar septa in COPD patients. External 16HBE treatment with BMP4 protein reduced the bronchial epithelial cell proliferation. Conclusions: These data show an imbalance between BMP proteins and their antagonists in the lungs of stable COPD. This imbalance may play a role in the remodeling of the airways, altering the regenerative–reparative responses of the diseased bronchioles and lung parenchyma. Full article

(This article belongs to the Special Issue Editorial Board Members' Collection Series: Cell Signaling in Health and Disease)

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Graphical abstract

11 pages, 2475 KiB

Open AccessArticle

N⁶-Methyladenosine Directly Regulates CD40L Expression in CD4⁺ T Lymphocytes

by Ellen C. N. van Vroonhoven, Lucas W. Picavet, Rianne C. Scholman, Noortje A. M. van den Dungen, Michal Mokry, Anouk Evers, Robert J. Lebbink, Jorg J. A. Calis, Sebastiaan J. Vastert and Jorg van Loosdregt

Biology 2023, 12(7), 1004; https://doi.org/10.3390/biology12071004 - 14 Jul 2023

Cited by 1 | Viewed by 1205

Abstract

T cell activation is a highly regulated process, modulated via the expression of various immune regulatory proteins including cytokines, surface receptors and co-stimulatory proteins. N⁶-methyladenosine (m⁶A) is an RNA modification that can directly regulate RNA expression levels and it is associated with various biological processes. However, the function of m⁶A in T cell activation remains incompletely understood. We identify m⁶A as a novel regulator of the expression of the CD40 ligand (CD40L) in human CD4⁺ lymphocytes. Manipulation of the m⁶A ‘eraser’ fat mass and obesity-associated protein (FTO) and m⁶A ‘writer’ protein methyltransferase-like 3 (METTL3) directly affects the expression of CD40L. The m⁶A ‘reader’ protein YT521-B homology domain family-2 (YTHDF2) is hypothesized to be able to recognize and bind m⁶A specific sequences on the CD40L mRNA and promotes its degradation. This study demonstrates that CD40L expression in human primary CD4⁺ T lymphocytes is regulated via m⁶A modifications, elucidating a new regulatory mechanism in CD4⁺ T cell activation that could possibly be leveraged in the future to modulate T cell responses in patients with immune-related diseases. Full article

(This article belongs to the Special Issue Editorial Board Members' Collection Series: Cell Signaling in Health and Disease)

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Review

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21 pages, 3477 KiB

Open AccessReview

Parathyroid Hormone Related Protein (PTHrP)-Associated Molecular Signatures in Tissue Differentiation and Non-Tumoral Diseases

by Mariangela Librizzi, Flores Naselli, Giulia Abruscato, Claudio Luparello and Fabio Caradonna

Biology 2023, 12(7), 950; https://doi.org/10.3390/biology12070950 - 03 Jul 2023

Cited by 1 | Viewed by 1810

Abstract

Parathyroid-hormone-related protein (PTHrP) is encoded by the PTHLH gene which, via alternative promoter usage and splicing mechanisms, can give rise to at least three isoforms of 139, 141, and 173 amino acids with distinct C-terminals. PTHrP is subjected to different post-translational processing that generates smaller bioactive forms, comprising amino terminus, mid-region (containing a nuclear/nucleolar targeting signal), and carboxy terminus peptides. Both the full-length protein and the discrete peptides are key controllers of viability, proliferation, differentiation, and apoptosis in diverse normal and pathological biological systems via the reprogramming of gene expression and remodulation of PKA or PKC-mediated signalization mechanisms. The aim of this review is to pick up selected studies on PTHrP-associated signatures as revealed by molecular profiling assays, focusing on the available data about exemplary differentiating, differentiated, or nontumoral cell and tissue models. In particular, the data presented relate to adipose, bone, dental, cartilaginous, and skin tissues, as well as intestinal, renal, hepatic, pulmonary, and pancreatic epithelia, with a focus on hepatic fibrosis-, pancreatitis-, and diabetes-related changes as diseased states. When reported, the biochemical and/or physiological aspects associated with the specific molecular modulation of gene expression and signal transduction pathways in the target model systems under examination are also briefly described. Full article

(This article belongs to the Special Issue Editorial Board Members' Collection Series: Cell Signaling in Health and Disease)

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11 pages, 640 KiB

Open AccessReview

Histopathology of Skeletal Muscle in a Distal Motor Neuropathy Associated with a Mutant CCT5 Subunit: Clues for Future Developments to Improve Differential Diagnosis and Personalized Therapy

by Federica Scalia, Everly Conway de Macario, Giuseppe Bonaventura, Francesco Cappello and Alberto J. L. Macario

Biology 2023, 12(5), 641; https://doi.org/10.3390/biology12050641 - 23 Apr 2023

Viewed by 1526

Abstract

Genetic chaperonopathies are rare but, because of misdiagnosis, there are probably more cases than those that are recorded in the literature and databases. This occurs because practitioners are generally unaware of the existence and/or the symptoms and signs of chaperonopathies. It is necessary to educate the medical community about these diseases and, with research, to unveil their mechanisms. The structure and functions of various chaperones in vitro have been studied, but information on the impact of mutant chaperones in humans, in vivo, is scarce. Here, we present a succinct review of the most salient abnormalities of skeletal muscle, based on our earlier report of a patient who carried a mutation in the chaperonin CCT5 subunit and suffered from a distal motor neuropathy of early onset. We discuss our results in relation to the very few other published pertinent reports we were able to find. A complex picture of multiple muscle-tissue abnormalities was evident, with signs of atrophy, apoptosis, and abnormally low levels and atypical distribution patterns of some components of muscle and the chaperone system. In-silico analysis predicts that the mutation affects CCT5 in a way that could interfere with the recognition and handling of substrate. Thus, it is possible that some of the abnormalities are the direct consequence of defective chaperoning, but others may be indirectly related to defective chaperoning or caused by other different pathogenic pathways. Biochemical, and molecular biologic and genetic analyses should now help in understanding the mechanisms underpinning the histologic abnormalities and, thus, provide clues to facilitate diagnosis and guide the development of therapeutic tools. Full article

(This article belongs to the Special Issue Editorial Board Members' Collection Series: Cell Signaling in Health and Disease)

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