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Biomedicines
Special Issues
Editorial Board Members' Collection Series: Gene and Cell Therapy
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Editorial Board Members' Collection Series: Gene and Cell Therapy

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

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 4155

Special Issue Editors

Dr. Agnes Klar

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Guest Editor
Tissue Biology Research Unit, Department of Surgery, University Children’s Hospital Zurich, 8032 Zurich, Switzerland
Interests: human skin; keratinocytes; endothelial cells; skin substitutes; stem cells; melanocytes; adipose-dervied stem cells; fat tissue; skin inflammation; immune cells; skin adipocyte progenitors
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Antonio Gomez-Muñoz

E-Mail Website
Guest Editor
Departamento de Bioquímica y Biología Molecular, Facultad de Ciencias y Tecnología, Universidad del Pais Vasco - Euskal Herriko Unibertsitatea, Campus Bizkaia, Leioa, Spain
Interests: adipogenesis; cell proliferation and survival; cell migration/invasion; sphingolipids, ceramides, ceramide kinase; inflammation

Special Issue Information

Dear Colleagues,

We are pleased to announce this collection entitled “Editorial Board Members’ Collection Series: Gene and Cell Therapy”. This 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 gene and cell therapy. All papers will be fully open access upon publication after peer review.

Dr. Agnes Klar
Prof. Dr. Antonio Gomez-Muñoz
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.

Keywords

  • gene therapy
  • cell therapy
  • stem cell therapy
  • tissue engineering
  • regenerative medicine
  • genomic medicine
  • animal models
  • genome editing
  • RNA therapeutics

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  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (2 papers)

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Research

22 pages, 5800 KiB  
Article
BHLHE40 Maintains the Stemness of PαS Cells In Vitro by Targeting Zbp1 through the Wnt/β-Catenin Signaling Pathway
by Menglong Hu, Yueming Tian, Xuenan Liu, Qian Guo, Dazhuang Lu, Xu Wang, Longwei Lv, Xiao Zhang, Yunsong Liu, Yongsheng Zhou and Ping Zhang
Biomedicines 2023, 11(8), 2190; https://doi.org/10.3390/biomedicines11082190 - 3 Aug 2023
Cited by 1 | Viewed by 1528
Abstract
Primary bone mesenchymal stem cells (BMSCs) gradually lose stemness during in vitro expansion, which significantly affects the cell therapeutic effects. Here, we chose murine PαS (SCA-1+PDGFRα+CD45−TER119−) cells as representative of BMSCs and aimed to explore [...] Read more.
Primary bone mesenchymal stem cells (BMSCs) gradually lose stemness during in vitro expansion, which significantly affects the cell therapeutic effects. Here, we chose murine PαS (SCA-1+PDGFRα+CD45−TER119−) cells as representative of BMSCs and aimed to explore the premium culture conditions for PαS cells. Freshly isolated (fresh) PαS cells were obtained from the limbs of C57/6N mice by fluorescence-activated cell sorting (FACS). We investigated the differences in the stemness of PαS cells by proliferation, differentiation, and stemness markers in vitro and by ectopic osteogenesis and chondrogenesis ability in vivo, as well as the changes in the stemness of PαS cells during expansion in vitro. Gain- and loss-of-function experiments were applied to investigate the critical role and underlying mechanism of the basic helix–loop–helix family member E40 (BHLHE40) in maintaining the stemness of PαS cells. The stemness of fresh PαS cells representative in vivo was superior to that of passage 0 (P0) PαS cells in vitro. The stemness of PαS cells in vitro decreased gradually from P0 to passage 4 (P4). Moreover, BHLHE40 plays a critical role in regulating the stemness of PαS cells during in vitro expansion. Mechanically, BHLHE40 regulates the stemness of PαS cells by targeting Zbp1 through the Wnt/β-catenin signaling pathway. This work confirms that BHLHE40 is a critical factor for regulating the stemness of PαS cells during expansion in vitro and may provide significant indications in the exploration of premium culture conditions for PαS cells. Full article
(This article belongs to the Special Issue Editorial Board Members' Collection Series: Gene and Cell Therapy)
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18 pages, 3457 KiB  
Article
Phosphatidic Acid Stimulates Lung Cancer Cell Migration through Interaction with the LPA1 Receptor and Subsequent Activation of MAP Kinases and STAT3
by Ana Gomez-Larrauri, Patricia Gangoiti, Laura Camacho, Natalia Presa, Cesar Martin and Antonio Gomez-Muñoz
Biomedicines 2023, 11(7), 1804; https://doi.org/10.3390/biomedicines11071804 - 23 Jun 2023
Cited by 4 | Viewed by 2052
Abstract
Phosphatidic acid (PA) is a key bioactive glycerophospholipid that is implicated in the regulation of vital cell functions such as cell growth, differentiation, and migration, and is involved in a variety of pathologic processes. However, the molecular mechanisms by which PA exerts its [...] Read more.
Phosphatidic acid (PA) is a key bioactive glycerophospholipid that is implicated in the regulation of vital cell functions such as cell growth, differentiation, and migration, and is involved in a variety of pathologic processes. However, the molecular mechanisms by which PA exerts its pathophysiological actions are incompletely understood. In the present work, we demonstrate that PA stimulates the migration of the human non-small cell lung cancer (NSCLC) A549 adenocarcinoma cells, as determined by the transwell migration assay. PA induced the rapid phosphorylation of mitogen-activated protein kinases (MAPKs) ERK1-2, p38, and JNK, and the pretreatment of cells with selective inhibitors of these kinases blocked the PA-stimulated migration of cancer cells. In addition, the chemotactic effect of PA was inhibited by preincubating the cells with pertussis toxin (PTX), a Gi protein inhibitor, suggesting the implication of a Gi protein-coupled receptor in this action. Noteworthy, a blockade of LPA receptor 1 (LPA1) with the specific LPA1 antagonist AM966, or with the selective LPA1 inhibitors Ki1645 or VPC32193, abolished PA-stimulated cell migration. Moreover, PA stimulated the phosphorylation of the transcription factor STAT3 downstream of JAK2, and inhibitors of either JAK2 or STAT3 blocked PA-stimulated cell migration. It can be concluded that PA stimulates lung adenocarcinoma cell migration through an interaction with the LPA1 receptor and subsequent activation of the MAPKs ERK1-2, p38, and JNK, and that the JAK2/STAT3 pathway is also important in this process. These findings suggest that targeting PA formation and/or the LPA1 receptor may provide new strategies to reduce malignancy in lung cancer. Full article
(This article belongs to the Special Issue Editorial Board Members' Collection Series: Gene and Cell Therapy)
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