Submit to Biomedicines Review for Biomedicines Propose a Special Issue

Journal Browser

Editorial Board Members' Collection Series: Cell Biology and Pathology

Print Special Issue Flyer
Special Issue Editors
Special Issue Information
Published Papers

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 14879

Share This Special Issue

Special Issue Editors

Dr. Pedro A. José

E-Mail Website
Guest Editor

Medicine and Physiology/Pharmacology, School of Medicine and Health Sciences, The George Washington University, Washington, DC, USA
Interests: hypertension; renal physiology; ion transport; oxidative stress; pharmacogenomics
Special Issues, Collections and Topics in MDPI journals

Dr. Georgia Levidou

E-Mail Website
Guest Editor

Department of Pathology, Paracelsus Medical University, 90419 Nuremberg, Germany
Interests: molecular pathology; immunohistochemistry; biomarkers; cancer; melanoma; lymphoma; thymic epithelial tumors; epigenetic factors; metastasis; targeted therapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to announce this collection entitled “Editorial Board Members’ Collection Series: Cell Biology and Pathology”. This Special Issue will be a collection of papers by researchers invited by the Editorial Board Members. The aim is to provide a venue for networking and communication between biomedicines and scholars in the field of cell biology and pathology. All papers will be fully open access upon publication after peer review.

Dr. Pedro A. José
Dr. Georgia Levidou
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. Biomedicines 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 2600 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.

Published Papers (10 papers)

Download All Papers

Research

Jump to: Review

11 pages, 627 KiB

Open AccessArticle

Elevated NET, Calprotectin, and Neopterin Levels Discriminate between Disease Activity in COVID-19, as Evidenced by Need for Hospitalization among Patients in Northern Italy

by Geir Hetland, Magne Kristoffer Fagerhol, Mohammad Reza Mirlashari, Lise Sofie Haug Nissen-Meyer, Stefania Croci, Paola Adele Lonati, Martina Bonacini, Carlo Salvarani, Chiara Marvisi, Caterina Bodio, Francesco Muratore, Maria Orietta Borghi and Pier Luigi Meroni

Biomedicines 2024, 12(4), 766; https://doi.org/10.3390/biomedicines12040766 - 30 Mar 2024

Viewed by 533

Abstract

Coronavirus disease 2019 (COVID-19) displays clinical heterogeneity, but little information is available for patients with mild or very early disease. We aimed to characterize biomarkers that are useful for discriminating the hospitalization risk in a COVID-19 cohort from Northern Italy during the first pandemic wave. We enrolled and followed for four weeks 76 symptomatic SARS-CoV-2 positive patients and age/sex-matched healthy controls. Patients with mild disease were discharged (n.42), and the remaining patients were hospitalized (n.34). Blood was collected before any anti-inflammatory/immunosuppressive therapy and assessed for soluble C5b-9/C5a, H3-neutrophil extracellular traps (NETs), calprotectin, and DNase plasma levels via ELISA and a panel of proinflammatory cytokines via ELLA. Calprotectin and NET levels discriminate between hospitalized and non-hospitalized patients, while DNase negatively correlates with NET levels; there are positive correlations between calprotectin and both NET and neopterin levels. Neopterin levels increase in patients at the beginning of the disease and do so more in hospitalized than non-hospitalized patients. C5a and sC5b-9, and other acute phase proteins, correlate with neopterin, calprotectin, and DNase. Both NET and neopterin levels negatively correlate with platelet count. We show that calprotectin, NETs, and neopterin are important proinflammatory parameters potentially useful for discriminating between COVID-19 patients at risk of hospitalization. Full article

(This article belongs to the Special Issue Editorial Board Members' Collection Series: Cell Biology and Pathology)

► Show Figures

Figure 1

18 pages, 1677 KiB

Open AccessArticle

USP7 Deregulation Impairs S Phase Specific DNA Repair after Irradiation in Breast Cancer Cells

by Marie Vogt, Sandra Classen, Ann Kristin Krause, Nadja-Juanita Peter, Cordula Petersen, Kai Rothkamm, Kerstin Borgmann and Felix Meyer

Biomedicines 2024, 12(4), 762; https://doi.org/10.3390/biomedicines12040762 - 29 Mar 2024

Viewed by 595

Abstract

The ubiquitin specific protease 7 (USP7) is a deubiquitinating enzyme with numerous substrates. Aberrant expression of USP7 is associated with tumor progression. This study aims to investigate how a deregulated USP7 expression affects chromosomal instability and prognosis of breast cancer patients in silico and radiosensitivity and DNA repair in breast cancer cells in vitro. The investigations in silico were performed using overall survival and USP7 mRNA expression data of breast cancer patients. The results showed that a high USP7 expression was associated with increased chromosomal instability and decreased overall survival. The in vitro experiments were performed in a luminal and a triple-negative breast cancer cell line. Proliferation, DNA repair, DNA replication stress, and survival after USP7 overexpression or inhibition and irradiation were analyzed. Both, USP7 inhibition and overexpression resulted in decreased cellular survival, distinct radiosensitization and an increased number of residual DNA double-strand breaks in the S phase following irradiation. RAD51 recruitment and base incorporation were decreased after USP7 inhibition plus irradiation and more single-stranded DNA was detected. The results show that deregulation of USP7 activity disrupts DNA repair in the S phase by increasing DNA replication stress and presents USP7 as a promising target to overcome the radioresistance of breast tumors. Full article

(This article belongs to the Special Issue Editorial Board Members' Collection Series: Cell Biology and Pathology)

► Show Figures

Figure 1

15 pages, 2043 KiB

Open AccessArticle

The Human Soluble NKG2D Ligand Differentially Impacts Tumorigenicity and Progression in Temporal and Model-Dependent Modes

by Anthony V. Serritella, Pablo Saenz-Lopez Larrocha, Payal Dhar, Sizhe Liu, Milan M. Medd, Shengxian Jia, Qi Cao and Jennifer D. Wu

Biomedicines 2024, 12(1), 196; https://doi.org/10.3390/biomedicines12010196 - 16 Jan 2024

Viewed by 919

Abstract

NKG2D is an activating receptor expressed by all human NK cells and CD8 T cells. Harnessing the NKG2D/NKG2D ligand axis has emerged as a viable avenue for cancer immunotherapy. However, there is a long-standing controversy over whether soluble NKG2D ligands are immunosuppressive or immunostimulatory, originating from conflicting data generated from different scopes of pre-clinical investigations. Using multiple pre-clinical tumor models, we demonstrated that the impact of the most characterized human solid tumor-associated soluble NKG2D ligand, the soluble MHC I chain-related molecule (sMIC), on tumorigenesis depended on the tumor model being studied and whether the tumor cells possessed stemness-like properties. We demonstrated that the potential of tumor formation or establishment depended upon tumor cell stem-like properties irrespective of tumor cells secreting the soluble NKG2D ligand sMIC. Specifically, tumor formation was delayed or failed if sMIC-expressing tumor cells expressed low stem-cell markers; tumor formation was rapid if sMIC-expressing tumor cells expressed high stem-like cell markers. However, once tumors were formed, overexpression of sMIC unequivocally suppressed tumoral NK and CD8 T cell immunity and facilitated tumor growth. Our study distinguished the differential impacts of soluble NKG2D ligands in tumor formation and tumor progression, cleared the outstanding controversy over soluble NKG2D ligands in modulating tumor immunity, and re-enforced the viability of targeting soluble NKG2D ligands for cancer immunotherapy for established tumors. Full article

(This article belongs to the Special Issue Editorial Board Members' Collection Series: Cell Biology and Pathology)

► Show Figures

Figure 1

20 pages, 9721 KiB

Open AccessArticle

Preclinical Efficacy of Peripheral Nerve Regeneration by Schwann Cell-like Cells Differentiated from Human Tonsil-Derived Mesenchymal Stem Cells in C22 Mice

by Yu Hwa Nam, Saeyoung Park, Yoonji Yum, Soyeon Jeong, Hyo Eun Park, Ho Jin Kim, Jaeseung Lim, Byung-Ok Choi and Sung-Chul Jung

Biomedicines 2023, 11(12), 3334; https://doi.org/10.3390/biomedicines11123334 - 17 Dec 2023

Cited by 1 | Viewed by 1504

Abstract

Charcot–Marie–Tooth disease (CMT) is a hereditary disease with heterogeneous phenotypes and genetic causes. CMT type 1A (CMT1A) is a type of disease affecting the peripheral nerves and is caused by the duplication of the peripheral myelin protein 22 (PMP22) gene. Human tonsil-derived mesenchymal stem cells (TMSCs) are useful for stem cell therapy in various diseases and can be differentiated into Schwann cell-like cells (TMSC-SCs). We investigated the potential of TMSC-SCs called neuronal regeneration-promoting cells (NRPCs) for peripheral nerve and muscle regeneration in C22 mice, a model for CMT1A. We transplanted NRPCs manufactured in a good manufacturing practice facility into the bilateral thigh muscles of C22 mice and performed behavior and nerve conduction tests and histological and ultrastructural analyses. Significantly, the motor function was much improved, the ratio of myelinated axons was increased, and the G-ratio was reduced by the transplantation of NRPCs. The sciatic nerve and gastrocnemius muscle regeneration of C22 mice following the transplantation of NRPCs downregulated PMP22 overexpression, which was observed in a dose-dependent manner. These results suggest that NRPCs are feasible for clinical research for the treatment of CMT1A patients. Research applying NRPCs to other peripheral nerve diseases is also needed. Full article

(This article belongs to the Special Issue Editorial Board Members' Collection Series: Cell Biology and Pathology)

► Show Figures

Figure 1

12 pages, 2773 KiB

Open AccessArticle

c-Met⁺ Cytotoxic T Lymphocytes Exhibit Enhanced Cytotoxicity in Mice and Humans In Vitro Tumor Models

by Mahdia Benkhoucha, Ngoc Lan Tran, Isis Senoner, Gautier Breville, Hajer Fritah, Denis Migliorini, Valérie Dutoit and Patrice H. Lalive

Biomedicines 2023, 11(12), 3123; https://doi.org/10.3390/biomedicines11123123 - 23 Nov 2023

Viewed by 854

Abstract

CD8⁺ cytotoxic T lymphocytes (CTLs) play a crucial role in anti-tumor immunity. In a previous study, we identified a subset of murine effector CTLs expressing the hepatocyte growth factor (HGF) receptor, c-Met (c-Met⁺ CTLs), that are endowed with enhanced cytolytic capacity. HGF directly inhibited the cytolytic function of c-Met⁺ CTLs, both in 2D in vitro assays and in vivo, leading to reduced T cell responses against metastatic melanoma. To further investigate the role of c-Met⁺ CTLs in a three-dimensional (3D) setting, we studied their function within B16 melanoma spheroids and examined the impact of cell–cell contact on the modulation of inhibitory checkpoint molecules’ expression, such as KLRG1, PD-1, and CTLA-4. Additionally, we evaluated the cytolytic capacity of human CTL clones expressing c-Met (c-Met⁺) and compared it to c-Met⁻ CTL clones. Our results indicated that, similar to their murine counterparts, c-Met⁺ human CTL clones exhibited increased cytolytic activity compared to c-Met⁻ CTL clones, and this enhanced function was negatively regulated by the presence of HGF. Taken together, our findings highlight the potential of targeting the HGF/c-Met pathway to modulate CTL-mediated anti-tumor immunity. This research holds promise for developing strategies to enhance the effectiveness of CTL-based immunotherapies against cancer. Full article

(This article belongs to the Special Issue Editorial Board Members' Collection Series: Cell Biology and Pathology)

► Show Figures

Figure 1

20 pages, 2120 KiB

Open AccessArticle

Regulation of Soluble E-Cadherin Signaling in Non-Small-Cell Lung Cancer Cells by Nicotine, BDNF, and β-Adrenergic Receptor Ligands

by Ravel Ray, Stuti Goel, Hind Al Khashali, Ban Darweesh, Ben Haddad, Caroline Wozniak, Robert Ranzenberger, Jeneen Khalil, Jeffrey Guthrie, Deborah Heyl and Hedeel Guy Evans

Biomedicines 2023, 11(9), 2555; https://doi.org/10.3390/biomedicines11092555 - 18 Sep 2023

Cited by 2 | Viewed by 1238

Abstract

The ectodomain of the transmembrane protein E-cadherin can be cleaved and released in a soluble form referred to as soluble E-cadherin, or sE-cad, accounting for decreased E-cadherin levels at the cell surface. Among the proteases implicated in this cleavage are matrix metalloproteases (MMP), including MMP9. Opposite functions have been reported for full-length E-cadherin and sE-cad. In this study, we found increased MMP9 levels in the media of two non-small cell lung cancer (NSCLC) cell lines, A549 and H1299, treated with BDNF, nicotine, or epinephrine that were decreased upon cell treatment with the β-adrenergic receptor blocker propranolol. Increased MMP9 levels correlated with increased sE-cad levels in A549 cell media, and knockdown of MMP9 in A549 cells led to downregulation of sE-cad levels in the media. Previously, we reported that A549 and H1299 cell viability increased with nicotine and/or BDNF treatment and decreased upon treatment with propranolol. In investigating the function of sE-cad, we found that immunodepletion of sE-cad from the media of A549 cells untreated or treated with BDNF, nicotine, or epinephrine reduced activation of EGFR and IGF-1R, decreased PI3K and ERK1/2 activities, increased p53 activation, decreased cell viability, and increased apoptosis, while no effects were found using H1299 cells under all conditions tested. Full article

(This article belongs to the Special Issue Editorial Board Members' Collection Series: Cell Biology and Pathology)

► Show Figures

Figure 1

11 pages, 2007 KiB

Open AccessArticle

SOX11 and Epithelial-Mesenchymal Transition in Metastatic Serous Ovarian Cancer

by Iason Psilopatis, Jule Ida Schaefer, Dimitrios Arsenakis, Dimitrios Bolovis and Georgia Levidou

Biomedicines 2023, 11(9), 2540; https://doi.org/10.3390/biomedicines11092540 - 15 Sep 2023

Viewed by 898

Abstract

Background: Ovarian cancer is the leading cause of death from gynecological malignancies, with serous carcinoma being the most common histopathologic subtype. Epithelial–mesenchymal transition (EMT) correlates with increased metastatic potential, whereas the transcription factor SRY-box transcription factor 11 (SOX11) is overexpressed in diverse malignancies. Methods: In the present study, we aimed to evaluate the potential role of the immunohistochemical expression of SOX11 in 30 serous ovarian carcinomas in association with E-cadherin and vimentin expression as well as with patients’ clinicopathological data. Results: Most of the examined cases showed concurrent expression of E-cadherin and vimentin, whereas SOX11 was expressed in a minority of the cases (26.7%). Interestingly, the positive cases more frequently had a metastatic disease at the time of diagnosis compared with the negative cases (p = 0.09), an association, however, of marginal significance. Moreover, there was a negative correlation between E-cadherin and SOX11 expression (p = 0.0077) and a positive correlation between vimentin and SOX11 expression (p = 0.0130). Conclusions: The present work, for the first time, provides preliminary evidence of a possible implication of SOX11 overexpression in the promotion of EMT in metastatic serous ovarian cancer, thereby endorsing tumor metastasis. Full article

(This article belongs to the Special Issue Editorial Board Members' Collection Series: Cell Biology and Pathology)

► Show Figures

Figure 1

Review

Jump to: Research

16 pages, 1604 KiB

Open AccessReview

Evaluation of Current Studies to Elucidate Processes in Dental Follicle Cells Driving Osteogenic Differentiation

by Christian Morsczeck, Michela De Pellegrin, Anja Reck and Torsten E. Reichert

Biomedicines 2023, 11(10), 2787; https://doi.org/10.3390/biomedicines11102787 - 13 Oct 2023

Viewed by 877

Abstract

When research on osteogenic differentiation in dental follicle cells (DFCs) began, projects focused on bone morphogenetic protein (BMP) signaling. The BMP pathway induces the transcription factor DLX3, whichh in turn induces the BMP signaling pathway via a positive feedback mechanism. However, this BMP2/DLX3 signaling pathway only seems to support the early phase of osteogenic differentiation, since simultaneous induction of BMP2 or DLX3 does not further promote differentiation. Recent data showed that inhibition of classical protein kinase C (PKCs) supports the mineralization of DFCs and that osteogenic differentiation is sensitive to changes in signaling pathways, such as protein kinase B (PKB), also known as AKT. Small changes in the lipidome seem to confirm the participation of AKT and PKC in osteogenic differentiation. In addition, metabolic processes, such as fatty acid biosynthesis, oxidative phosphorylation, or glycolysis, are essential for the osteogenic differentiation of DFCs. This review article attempts not only to bring the various factors into a coherent picture of osteogenic differentiation in DFCs, but also to relate them to recent developments in other types of osteogenic progenitor cells. Full article

(This article belongs to the Special Issue Editorial Board Members' Collection Series: Cell Biology and Pathology)

► Show Figures

Figure 1

22 pages, 4659 KiB

Open AccessReview

Updates in Glioblastoma Immunotherapy: An Overview of the Current Clinical and Translational Scenario

by Andrea Bianconi, Giuseppe Palmieri, Gelsomina Aruta, Matteo Monticelli, Pietro Zeppa, Fulvio Tartara, Antonio Melcarne, Diego Garbossa and Fabio Cofano

Biomedicines 2023, 11(6), 1520; https://doi.org/10.3390/biomedicines11061520 - 24 May 2023

Cited by 7 | Viewed by 3271

Abstract

Glioblastoma (GBM) is the most common and aggressive central nervous system tumor, requiring multimodal management. Due to its malignant behavior and infiltrative growth pattern, GBM is one of the most difficult tumors to treat and gross total resection is still considered to be the first crucial step. The deep understanding of GBM microenvironment and the possibility of manipulating the patient’s innate and adaptive immune system to fight the neoplasm represent the base of immunotherapeutic strategies that currently express the future for the fight against GBM. Despite the immunotherapeutic approach having been successfully adopted in several solid and haematologic neoplasms, immune resistance and the immunosuppressive environment make the use of these strategies challenging in GBM treatment. We describe the most recent updates regarding new therapeutic strategies that target the immune system, immune checkpoint inhibitors, chimeric antigen receptor T cell therapy, peptide and oncolytic vaccines, and the relevant mechanism of immune resistance. However, no significant results have yet been obtained in studies targeting single molecules/pathways. The future direction of GBM therapy will include a combined approach that, in contrast to the inescapable current treatment modality of maximal resection followed by chemo- and radiotherapy, may combine a multifaceted immunotherapy treatment with the dual goals of directly killing tumor cells and activating the innate and adaptive immune response. Full article

(This article belongs to the Special Issue Editorial Board Members' Collection Series: Cell Biology and Pathology)

► Show Figures

Figure 1

19 pages, 675 KiB

Open AccessReview

Patient-Derived Organoids: The Beginning of a New Era in Ovarian Cancer Disease Modeling and Drug Sensitivity Testing

by Iason Psilopatis, Alexandros G. Sykaras, Georgios Mandrakis, Kleio Vrettou and Stamatios Theocharis

Biomedicines 2023, 11(1), 1; https://doi.org/10.3390/biomedicines11010001 - 20 Dec 2022

Cited by 8 | Viewed by 2717

Abstract

Ovarian cancer (OC) is the leading cause of death from gynecological malignancies. Despite great advances in treatment strategies, therapeutic resistance and the gap between preclinical data and actual clinical efficacy justify the necessity of developing novel models for investigating OC. Organoids represent revolutionary three-dimensional cell culture models, deriving from stem cells and reflecting the primary tissue’s biology and pathology. The aim of the current review is to study the current status of mouse- and patient-derived organoids, as well as their potential to model carcinogenesis and perform drug screenings for OC. Herein, we describe the role of organoids in the assessment of high-grade serous OC (HGSOC) cells-of-origin, illustrate their use as promising preclinical OC models and highlight the advantages of organoid technology in terms of disease modelling and drug sensitivity testing. Full article

(This article belongs to the Special Issue Editorial Board Members' Collection Series: Cell Biology and Pathology)

► Show Figures

Figure 1

Journal Menu

Journal Browser

Editorial Board Members' Collection Series: Cell Biology and Pathology

Share This Special Issue

Special Issue Editors

Special Issue Information

Published Papers (10 papers)

Research

Review

Further Information

Guidelines

MDPI Initiatives

Follow MDPI