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Molecular Roadblocks for Cellular Differentiation, Transdifferentiation or Conversion
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Molecular Roadblocks for Cellular Differentiation, Transdifferentiation or Conversion

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (15 July 2021) | Viewed by 9084

Special Issue Editors

Prof. Dr. Simona Chera

E-Mail Website
Guest Editor
1. Department of Clinical Science, University of Bergen, Bergen, Norway
2. Division of Endocrinology, Diabetes, Nutrition, Faculty of Medicine, University of Geneva, 1205 Geneva, Switzerland
Interests: cell fate; cell conversion; regeneration; molecular networks
Special Issues, Collections and Topics in MDPI journals
Dr. Luiza Ghila

E-Mail Website
Guest Editor
Department of Cell Physiology and Metabolism, Faculty of Medicine, University of Geneva, 1205 Geneva, Switzerland
Interests: hiPSC; differentiation; transgenic models; pancreatic islet biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

At all stages of life, cells are continuously subjected to the influence of various factors, usually originating from within the close cellular environment or niche. Maintaining the cell identity can therefore be viewed as an active process counteracting the natural trend to change, and not a passive immovable cellular state. It can be postulated that the regulation of cell fate maintenance is under the influence of molecular roadblocks opposing the intrinsic and extrinsic factors promoting the change. The modulation of these “cell conversion breaks” could prove crucial for treating pathologies characterized by massive cell decay. Moreover, understanding these molecular roadblocks will also improve the in vitro differentiation protocols by uncovering molecular inhibitory signals regulating cell fate switches.

This Special Issue in Genes on “Molecular Roadblocks for Cellular Differentiation, Transdifferentiation or Conversion” will address the responding mechanisms to instructive signals, with a focus on molecular brakes regulating cell identity, and thus impacting tissue regeneration or cell differentiation, as described in different experimental models.

Prof. Dr. Simona Chera
Dr. Luiza Ghila
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. Genes 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

  • Cell differentiation
  • Transdifferentiation
  • Cell conversion
  • Regeneration
  • Molecular networks

Published Papers (2 papers)

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Research

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16 pages, 2296 KiB  
Article
Genetic and Epigenetic Modification of Rat Liver Progenitor Cells via HNF4α Transduction and 5’ Azacytidine Treatment: An Integrated miRNA and mRNA Expression Profile Analysis
by Jennifer Bolleyn, Matthias Rombaut, Nisha Nair, Steven Branson, Anja Heymans, Marinee Chuah, Thierry VandenDriessche, Vera Rogiers, Joery De Kock and Tamara Vanhaecke
Genes 2020, 11(5), 486; https://doi.org/10.3390/genes11050486 - 29 Apr 2020
Cited by 2 | Viewed by 3166
Abstract
Neonatal liver-derived rat epithelial cells (rLEC) from biliary origin are liver progenitor cells that acquire a hepatocyte-like phenotype upon sequential exposure to hepatogenic growth factors and cytokines. Undifferentiated rLEC express several liver-enriched transcription factors, including the hepatocyte nuclear factors (HNF) 3β and HNF6, [...] Read more.
Neonatal liver-derived rat epithelial cells (rLEC) from biliary origin are liver progenitor cells that acquire a hepatocyte-like phenotype upon sequential exposure to hepatogenic growth factors and cytokines. Undifferentiated rLEC express several liver-enriched transcription factors, including the hepatocyte nuclear factors (HNF) 3β and HNF6, but not the hepatic master regulator HNF4α. In this study, we first investigated the impact of the ectopic expression of HNF4α in rLEC on both mRNA and microRNA (miR) level by means of microarray technology. We found that HNF4α transduction did not induce major changes to the rLEC phenotype. However, we next investigated the influence of DNA methyl transferase (DNMT) inhibition on the phenotype of undifferentiated naïve rLEC by exposure to 5′ azacytidine (AZA), which was found to have a significant impact on rLEC gene expression. The transduction of HNF4α or AZA treatment resulted both in significantly downregulated C/EBPα expression levels, while the exposure of the cells to AZA had a significant effect on the expression of HNF3β. Computationally, dysregulated miRNAs were linked to target mRNAs using the microRNA Target Filter function of Ingenuity Pathway Analysis. We found that differentially regulated miRNA–mRNA target associations predict ectopic HNF4α expression in naïve rLEC to interfere with cell viability and cellular maturation (miR-19b-3p/NR4A2, miR30C-5p/P4HA2, miR328-3p/CD44) while it predicts AZA exposure to modulate epithelial/hepatic cell proliferation, apoptosis, cell cycle progression and the differentiation of stem cells (miR-18a-5p/ESR1, miR-503-5p/CCND1). Finally, our computational analysis predicts that the combination of HNF4α transduction with subsequent AZA treatment might cause changes in hepatic cell proliferation and maturation (miR-18a-5p/ESR1, miR-503-5p/CCND1, miR-328-3p/CD44) as well as the apoptosis (miR-16-5p/BCL2, miR-17-5p/BCL2, miR-34a-5p/BCL2 and miR-494-3p/HMOX1) of naïve rLEC. Full article
(This article belongs to the Special Issue Molecular Roadblocks for Cellular Differentiation, Transdifferentiation or Conversion)
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21 pages, 5691 KiB  
Review
Embryonic Kidney Development, Stem Cells and the Origin of Wilms Tumor
by Hao Li, Peter Hohenstein and Satu Kuure
Genes 2021, 12(2), 318; https://doi.org/10.3390/genes12020318 - 23 Feb 2021
Cited by 21 | Viewed by 5460
Abstract
The adult mammalian kidney is a poorly regenerating organ that lacks the stem cells that could replenish functional homeostasis similarly to, e.g., skin or the hematopoietic system. Unlike a mature kidney, the embryonic kidney hosts at least three types of lineage-specific stem cells [...] Read more.
The adult mammalian kidney is a poorly regenerating organ that lacks the stem cells that could replenish functional homeostasis similarly to, e.g., skin or the hematopoietic system. Unlike a mature kidney, the embryonic kidney hosts at least three types of lineage-specific stem cells that give rise to (a) a ureter and collecting duct system, (b) nephrons, and (c) mesangial cells together with connective tissue of the stroma. Extensive interest has been raised towards these embryonic progenitor cells, which are normally lost before birth in humans but remain part of the undifferentiated nephrogenic rests in the pediatric renal cancer Wilms tumor. Here, we discuss the current understanding of kidney-specific embryonic progenitor regulation in the innate environment of the developing kidney and the types of disruptions in their balanced regulation that lead to the formation of Wilms tumor. Full article
(This article belongs to the Special Issue Molecular Roadblocks for Cellular Differentiation, Transdifferentiation or Conversion)
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