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Cells
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Cell Biology: State-of-the-Art and Perspectives in Italy
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Cell Biology: State-of-the-Art and Perspectives in Italy

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (10 August 2023) | Viewed by 21527

Special Issue Editors

Dr. Vincenzo Carafa

E-Mail Website
Guest Editor
Department of Precision Medicine, University of Campania Luigi Vanvitelli, 80138 Napoli, Italy
Interests: programmed cell death; apoptosis; leukaemia; epigenetic; acetylation; sirtuins
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Lucia Altucci

E-Mail Website
Co-Guest Editor
Department of Precision Medicine, University of Campania Luigi Vanvitelli, 80138 Napoli, Italy
Interests: leukaemia; epigenetic; personalized medicine; networking approaches
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue aims to provide a comprehensive overview of the state of the art of cell biology in Italy. We invite research papers that will consolidate our understanding in this area. The Special Issue will publish full research articles and comprehensive reviews. Potential topics include but are not limited to the following research areas:

  • OMICS: transcriptomics, genomics, proteomics, metabolomics, glycomics, lipidomics, interactomics, fluxomics, and biomics;
  • Cell structure: organelles, cytoskeleton, cell membrane, capsule, flagella, etc.;
  • Cell physiology: cell growth, metabolism, protein synthesis, division, movement of proteins, active/passive transport, intra- and extracellular signaling, adhesion, DNA repair, etc.;
  • Cell movement and motility;
  • Autophagy;
  • Apoptosis;
  • PANoptosis;
  • Cell aging;
  • Cell techniques: cell and tissue culture, isolation, and fractionation of cells, immunocytochemistry (ICC), in situ hybridization (ISH), transfection, and optogenetics;
  • Cell growth and differentiation;
  • Hematopoiesis and stem cells;
  • Cancer stem cells;
  • Genetic disorders;
  • CAR-T cell research.

Dr. Vincenzo Carafa
Prof. Dr. Lucia Altucci
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. Cells is an international peer-reviewed open access semimonthly 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.

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Related Special Issues

Published Papers (7 papers)

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Research

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23 pages, 8157 KiB  
Article
Doxorubicin-Induced Cardiac Senescence Is Alleviated Following Treatment with Combined Polyphenols and Micronutrients through Enhancement in Mitophagy
by Eleonora Foglio, Erica D’Avorio, Laura Vitiello, Laura Masuelli, Roberto Bei, Francesca Pacifici, David Della-Morte, Simone Mirabilii, Maria Rosaria Ricciardi, Agostino Tafuri, Enrico Garaci, Matteo Antonio Russo, Marco Tafani and Federica Limana
Cells 2023, 12(22), 2605; https://doi.org/10.3390/cells12222605 - 10 Nov 2023
Cited by 1 | Viewed by 2555
Abstract
Oxidative stress and impaired mitophagy are the hallmarks of cardiomyocyte senescence. Specifically, a decrease in mitophagic flux leads to the accumulation of damaged mitochondria and the development of senescence through increased ROS and other mediators. In this study, we describe the preventive role [...] Read more.
Oxidative stress and impaired mitophagy are the hallmarks of cardiomyocyte senescence. Specifically, a decrease in mitophagic flux leads to the accumulation of damaged mitochondria and the development of senescence through increased ROS and other mediators. In this study, we describe the preventive role of A5+, a mix of polyphenols and other micronutrients, in doxorubicin (DOXO)-induced senescence of H9C2 cells. Specifically, H9C2 cells exposed to DOXO showed an increase in the protein expression proteins of senescence-associated genes, p21 and p16, and a decrease in the telomere binding factors TRF1 and TRF2, indicative of senescence induction. Nevertheless, A5+ pre-treatment attenuated the senescent-like cell phenotype, as evidenced by inhibition of all senescent markers and a decrease in SA-β-gal staining in DOXO-treated H9C2 cells. Importantly, A5+ restored the LC3 II/LC3 I ratio, Parkin and BNIP3 expression, therefore rescuing mitophagy, and decreased ROS production. Further, A5+ pre-treatment determined a ripolarization of the mitochondrial membrane and improved basal respiration. A5+-mediated protective effects might be related to its ability to activate mitochondrial SIRT3 in synergy with other micronutrients, but in contrast with SIRT4 activation. Accordingly, SIRT4 knockdown in H9C2 cells further increased MnSOD activity, enhanced mitophagy, and reduced ROS generation following A5+ pre-treatment and DOXO exposure compared to WT cells. Indeed, we demonstrated that A5+ protects H9C2 cells from DOXO-induced senescence, establishing a new specific role for A5+ in controlling mitochondrial quality control by restoring SIRT3 activity and mitophagy, which provided a molecular basis for the development of therapeutic strategies against cardiomyocyte senescence. Full article
(This article belongs to the Special Issue Cell Biology: State-of-the-Art and Perspectives in Italy)
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12 pages, 987 KiB  
Article
The Immune Response to SARS-CoV-2 Vaccine in a Cohort of Family Pediatricians from Southern Italy
by Paolo Cortese, Felice Amato, Antonio Davino, Raffaella De Franchis, Speranza Esposito, Immacolata Zollo, Marina Di Domenico, Egle Solito, Federica Zarrilli, Laura Gentile, Gustavo Cernera and Giuseppe Castaldo
Cells 2023, 12(11), 1447; https://doi.org/10.3390/cells12111447 - 23 May 2023
Cited by 5 | Viewed by 1959
Abstract
In Italy, from January 2021, the Ministry of Health indicated a vaccination plan against COVID for frail patients and physicians based on a three-dose scheme. However, conflicting results have been reported on which biomarkers permit immunization assessment. We used several laboratory approaches (i.e., [...] Read more.
In Italy, from January 2021, the Ministry of Health indicated a vaccination plan against COVID for frail patients and physicians based on a three-dose scheme. However, conflicting results have been reported on which biomarkers permit immunization assessment. We used several laboratory approaches (i.e., antibodies serum levels, flow cytometry analysis, and cytokines release by stimulated cells) to investigate the immune response in a cohort of 53 family pediatricians (FPs) at different times after the vaccine. We observed that the BNT162b2-mRNA vaccine induced a significant increase of specific antibodies after the third (booster) dose; however, the antibody titer was not predictive of the risk of developing the infection in the six months following the booster dose. The antigen stimulation of PBMC cells from subjects vaccinated with the third booster jab induced the increase of the activated T cells (i.e., CD4+ CD154+); the frequency of CD4+ CD154+ TNF-α+ cells, as well as the TNF-α secretion, was not modified, while we observed a trend of increase of IFN-γ secretion. Interestingly, the level of CD8+ IFN-γ+ (independently from antibody titer) was significantly increased after the third dose and predicts the risk of developing the infection in the six months following the booster jab. Such results may impact also other virus vaccinations. Full article
(This article belongs to the Special Issue Cell Biology: State-of-the-Art and Perspectives in Italy)
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14 pages, 2657 KiB  
Article
Androgens and NGF Mediate the Neurite-Outgrowth through Inactivation of RhoA
by Marzia Di Donato, Antonio Bilancio, Ferdinando Auricchio, Gabriella Castoria and Antimo Migliaccio
Cells 2023, 12(3), 373; https://doi.org/10.3390/cells12030373 - 19 Jan 2023
Cited by 5 | Viewed by 2582
Abstract
Steroid hormones and growth factors control neuritogenesis through their cognate receptors under physiological and pathological conditions. We have already shown that nerve growth factor and androgens induce neurite outgrowth of PC12 cells through a reciprocal crosstalk between the NGF receptor, TrkA and the [...] Read more.
Steroid hormones and growth factors control neuritogenesis through their cognate receptors under physiological and pathological conditions. We have already shown that nerve growth factor and androgens induce neurite outgrowth of PC12 cells through a reciprocal crosstalk between the NGF receptor, TrkA and the androgen receptor. Here, we report that androgens or NGF induce neuritogenesis in PC12 cells through inactivation of RhoA. Ectopic expression of the dominant negative RhoA N19 promotes, indeed, the neurite-elongation of unchallenged and androgen- or NGF-challenged PC12 cells and the increase in the expression levels of βIII tubulin, a specific neuronal marker. Pharmacological inhibition of the Ser/Thr kinase ROCK, an RhoA effector, induces neuritogenesis in unchallenged PC12 cells, and potentiates the effect of androgens and NGF, confirming the role of RhoA/ROCK axis in the neuritogenesis induced by androgen and NGF, through the phosphorylation of Akt. These findings suggest that therapies based on new selective androgen receptor modulators and/or RhoA/ROCK inhibitors might exert beneficial effects in the treatment of neuro-disorders, neurological diseases and ageing-related processes. Full article
(This article belongs to the Special Issue Cell Biology: State-of-the-Art and Perspectives in Italy)
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Review

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16 pages, 1144 KiB  
Review
The Melanocortin System in Inflammatory Bowel Diseases: Insights into Its Mechanisms and Therapeutic Potentials
by Antonietta Gerarda Gravina, Raffaele Pellegrino, Tommaso Durante, Giovanna Palladino, Giuseppe Imperio, Giovanbattista D’Amico, Maria Consiglia Trotta, Marcello Dallio, Mario Romeo, Michele D’Amico and Alessandro Federico
Cells 2023, 12(14), 1889; https://doi.org/10.3390/cells12141889 - 19 Jul 2023
Cited by 9 | Viewed by 1991
Abstract
The melanocortin system is a complex set of molecular mediators and receptors involved in many physiological and homeostatic processes. These include the regulation of melanogenesis, steroidogenesis, neuromodulation and the modulation of inflammatory processes. In the latter context, the system has assumed importance in [...] Read more.
The melanocortin system is a complex set of molecular mediators and receptors involved in many physiological and homeostatic processes. These include the regulation of melanogenesis, steroidogenesis, neuromodulation and the modulation of inflammatory processes. In the latter context, the system has assumed importance in conditions of chronic digestive inflammation, such as inflammatory bowel diseases (IBD), in which numerous experiences have been accumulated in mouse models of colitis. Indeed, information on how such a system can counteract colitis inflammation and intervene in the complex cytokine imbalance in the intestinal microenvironment affected by chronic inflammatory damage has emerged. This review summarises the evidence acquired so far and highlights that molecules interfering with the melanocortin system could represent new drugs for treating IBD. Full article
(This article belongs to the Special Issue Cell Biology: State-of-the-Art and Perspectives in Italy)
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14 pages, 1705 KiB  
Review
HAT1: Landscape of Biological Function and Role in Cancer
by Vincenza Capone, Laura Della Torre, Daniela Carannante, Mehrad Babaei, Lucia Altucci, Rosaria Benedetti and Vincenzo Carafa
Cells 2023, 12(7), 1075; https://doi.org/10.3390/cells12071075 - 2 Apr 2023
Cited by 5 | Viewed by 3228
Abstract
Histone modifications, as key chromatin regulators, play a pivotal role in the pathogenesis of several diseases, such as cancer. Acetylation, and more specifically lysine acetylation, is a reversible epigenetic process with a fundamental role in cell life, able to target histone and non-histone [...] Read more.
Histone modifications, as key chromatin regulators, play a pivotal role in the pathogenesis of several diseases, such as cancer. Acetylation, and more specifically lysine acetylation, is a reversible epigenetic process with a fundamental role in cell life, able to target histone and non-histone proteins. This epigenetic modification regulates transcriptional processes and protein activity, stability, and localization. Several studies highlight a specific role for HAT1 in regulating molecular pathways, which are altered in several pathologies, among which is cancer. HAT1 is the first histone acetyltransferase discovered; however, to date, its biological characterization is still unclear. In this review, we summarize and update the current knowledge about the biological function of this acetyltransferase, highlighting recent advances of HAT1 in the pathogenesis of cancer. Full article
(This article belongs to the Special Issue Cell Biology: State-of-the-Art and Perspectives in Italy)
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19 pages, 1407 KiB  
Review
Monocyte and Macrophage in Neuroblastoma: Blocking Their Pro-Tumoral Functions and Strengthening Their Crosstalk with Natural Killer Cells
by Chiara Vitale, Cristina Bottino and Roberta Castriconi
Cells 2023, 12(6), 885; https://doi.org/10.3390/cells12060885 - 13 Mar 2023
Cited by 7 | Viewed by 3597
Abstract
Over the past decade, immunotherapy has represented an enormous step forward in the fight against cancer. Immunotherapeutic approaches have increasingly become a fundamental part of the combined therapies currently adopted in the treatment of patients with high-risk (HR) neuroblastoma (NB). An increasing number [...] Read more.
Over the past decade, immunotherapy has represented an enormous step forward in the fight against cancer. Immunotherapeutic approaches have increasingly become a fundamental part of the combined therapies currently adopted in the treatment of patients with high-risk (HR) neuroblastoma (NB). An increasing number of studies focus on the understanding of the immune landscape in NB and, since this tumor expresses low or null levels of MHC class I, on the development of new strategies aimed at enhancing innate immunity, especially Natural Killer (NK) cells and macrophages. There is growing evidence that, within the NB tumor microenvironment (TME), tumor-associated macrophages (TAMs), which mainly present an M2-like phenotype, have a crucial role in mediating NB development and immune evasion, and they have been correlated to poor clinical outcomes. Importantly, TAM can also impair the antibody-dependent cellular cytotoxicity (ADCC) mediated by NK cells upon the administration of anti-GD2 monoclonal antibodies (mAbs), the current standard immunotherapy for HR-NB patients. This review deals with the main mechanisms regulating the crosstalk among NB cells and TAMs or other cellular components of the TME, which support tumor development and induce drug resistance. Furthermore, we will address the most recent strategies aimed at limiting the number of pro-tumoral macrophages within the TME, reprogramming the TAMs functional state, thus enhancing NK cell functions. We also prospectively discuss new or unexplored aspects of human macrophage heterogeneity. Full article
(This article belongs to the Special Issue Cell Biology: State-of-the-Art and Perspectives in Italy)
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35 pages, 3983 KiB  
Review
Emerging Roles of SIRT5 in Metabolism, Cancer, and SARS-CoV-2 Infection
by Emanuele Fabbrizi, Francesco Fiorentino, Vincenzo Carafa, Lucia Altucci, Antonello Mai and Dante Rotili
Cells 2023, 12(6), 852; https://doi.org/10.3390/cells12060852 - 9 Mar 2023
Cited by 22 | Viewed by 4494
Abstract
Sirtuin 5 (SIRT5) is a predominantly mitochondrial enzyme catalyzing the removal of glutaryl, succinyl, malonyl, and acetyl groups from lysine residues through a NAD+-dependent deacylase mechanism. SIRT5 is an important regulator of cellular homeostasis and modulates the activity of proteins involved [...] Read more.
Sirtuin 5 (SIRT5) is a predominantly mitochondrial enzyme catalyzing the removal of glutaryl, succinyl, malonyl, and acetyl groups from lysine residues through a NAD+-dependent deacylase mechanism. SIRT5 is an important regulator of cellular homeostasis and modulates the activity of proteins involved in different metabolic pathways such as glycolysis, tricarboxylic acid (TCA) cycle, fatty acid oxidation, electron transport chain, generation of ketone bodies, nitrogenous waste management, and reactive oxygen species (ROS) detoxification. SIRT5 controls a wide range of aspects of myocardial energy metabolism and plays critical roles in heart physiology and stress responses. Moreover, SIRT5 has a protective function in the context of neurodegenerative diseases, while it acts as a context-dependent tumor promoter or suppressor. In addition, current research has demonstrated that SIRT5 is implicated in the SARS-CoV-2 infection, although opposing conclusions have been drawn in different studies. Here, we review the current knowledge on SIRT5 molecular actions under both healthy and diseased settings, as well as its functional effects on metabolic targets. Finally, we revise the potential of SIRT5 as a therapeutic target and provide an overview of the currently reported SIRT5 modulators, which include both activators and inhibitors. Full article
(This article belongs to the Special Issue Cell Biology: State-of-the-Art and Perspectives in Italy)
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