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Cells
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Cell Biology Research in Germany: State-of-the-Art and Perspectives in Cellular...
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Cell Biology Research in Germany: State-of-the-Art and Perspectives in Cellular Pathology

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 8550

Special Issue Editors

Prof. Dr. Ritva Tikkanen

E-Mail Website
Guest Editor
Institute of Biochemistry, Medical Faculty, Justus-Liebig University of Giessen, Friedrichstrasse 24, D-35392 Giessen, Germany
Interests: lysosomal storage disorders; vesicular trafficking; endosomal sorting; lysosome biogenesis; mitochondrial diseases; autoimmune disorders
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Hassan Dihazi

E-Mail Website1 Website2
Guest Editor
1. Department of Nephrology and Rheumatology, Göttingen University Medical Center, Georg August University, Göttingen, Germany
2. Centre for Biostructural Imaging of Neurodegeneration (BIN), University Medical Center Göttingen, Georg August University, Göttingen, Germany
Interests: understanding the pathomechanisms of kidney diseases; investigating therapeutic targets for kidney fibrosis; ER stress proteins and UPR in kidney fibrosis; biomarker discovery and validation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

The COVID-19 pandemic not only affected everyday life but also enormously impacted the research community, who were obliged to deal with unexpected situations and face new challenges in their usual laboratory life. The cell biology community in Germany, in a similar manner to their colleagues worldwide, had to adapt and react to this new situation. Despite the challenging COVID-19 pandemic, the German cell biology community achieved pioneering work in the field of cellular pathology during this period. To honor the contribution of this community, we plan to dedicate a Special Issue in our journal Cells to cell biology research in Germany, especially the cellular pathology research conducted under the special conditions of the COVID-19 pandemic. This Special Issue aims to provide an overview of the state-of-the-art achievements in this field in Germany during recent years. We invite and encourage researchers to submit their high-quality research papers that will consolidate our understanding in this area. The Special Issue will publish full research articles and comprehensive reviews. We will be seeking a balance between high-quality review articles and original scientific reports in order to yield a Special Issue of broad interest for the cellular pathology community worldwide. To cover the broad field of cellular pathology the topics of our Special Issue include, but are not limited to, the following research areas: cell structure, cell physiology, cell metabolism, cell movement and motility, cell adhesion, cell biology techniques, omics in cellular pathology, cell growth and differentiation, cell apoptosis, and autophagy. 

Prof. Dr. Ritva Tikkanen
Prof. Dr. Hassan Dihazi
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.

Keywords

  • structural pathology of cells and matrices
  • cellular metabolism under pathologic conditions
  • cell physiology and pathophysiology
  • cellular senescence from physiology to pathology
  • normal and pathological cell motility
  • cell techniques (cell and tissue culture, isolation and fractionation of cells, immunocytochemistry (ICC), in situ hybridization (ISH), transfection, and optogenetics)
  • omics in investigating cellular pathology (transcriptomics, genomics, proteomics, metabolomics, glycomics, lipidomics, interactomics, etc.)
  • disorders of cellular growth and differentiation
  • genetic disorders

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Published Papers (3 papers)

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Research

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20 pages, 12217 KiB  
Article
Starvation Protects Hepatocytes from Inflammatory Damage through Paradoxical mTORC1 Signaling
by Iqra Hussain, Harini K. Sureshkumar, Michael Bauer and Ignacio Rubio
Cells 2023, 12(12), 1668; https://doi.org/10.3390/cells12121668 - 20 Jun 2023
Cited by 2 | Viewed by 1907 | Correction
Abstract
Background and aims: Sepsis-related liver failure is associated with a particularly unfavorable clinical outcome. Calorie restriction is a well-established factor that can increase tissue resilience, protect against liver failure and improve outcome in preclinical models of bacterial sepsis. However, the underlying molecular [...] Read more.
Background and aims: Sepsis-related liver failure is associated with a particularly unfavorable clinical outcome. Calorie restriction is a well-established factor that can increase tissue resilience, protect against liver failure and improve outcome in preclinical models of bacterial sepsis. However, the underlying molecular basis is difficult to investigate in animal studies and remains largely unknown. Methods: We have used an immortalized hepatocyte line as a model of the liver parenchyma to uncover the role of caloric restriction in the resilience of hepatocytes to inflammatory cell damage. In addition, we applied genetic and pharmacological approaches to investigate the contribution of the three major intracellular nutrient/energy sensor systems, AMPK, mTORC1 and mTORC2, in this context. Results: We demonstrate that starvation reliably protects hepatocytes from cellular damage caused by pro-inflammatory cytokines. While the major nutrient- and energy-related signaling pathways AMPK, mTORC2/Akt and mTORC1 responded to caloric restriction as expected, mTORC1 was paradoxically activated by inflammatory stress in starved, energy-deprived hepatocytes. Pharmacological inhibition of mTORC1 or genetic silencing of the mTORC1 scaffold Raptor, but not its mTORC2 counterpart Rictor, abrogated the protective effect of starvation and exacerbated inflammation-induced cell death. Remarkably, mTORC1 activation in starved hepatocytes was uncoupled from the regulation of autophagy, but crucial for sustained protein synthesis in starved resistant cells. Conclusions: AMPK engagement and paradoxical mTORC1 activation and signaling mediate protection against pro-inflammatory stress exerted by caloric restriction in hepatocytes. Full article
(This article belongs to the Special Issue Cell Biology Research in Germany: State-of-the-Art and Perspectives in Cellular Pathology)
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21 pages, 5927 KiB  
Article
Genetic Characterization of Rat Hepatic Stellate Cell Line HSC-T6 for In Vitro Cell Line Authentication
by Indrajit Nanda, Claus Steinlein, Thomas Haaf, Eva M. Buhl, Domink G. Grimm, Scott L. Friedman, Steffen K. Meurer, Sarah K. Schröder and Ralf Weiskirchen
Cells 2022, 11(11), 1783; https://doi.org/10.3390/cells11111783 - 29 May 2022
Cited by 11 | Viewed by 2928
Abstract
Immortalized hepatic stellate cells (HSCs) established from mouse, rat, and humans are valuable in vitro models for the biomedical investigation of liver biology. These cell lines are homogenous, thereby providing consistent and reproducible results. They grow more robustly than primary HSCs and provide [...] Read more.
Immortalized hepatic stellate cells (HSCs) established from mouse, rat, and humans are valuable in vitro models for the biomedical investigation of liver biology. These cell lines are homogenous, thereby providing consistent and reproducible results. They grow more robustly than primary HSCs and provide an unlimited supply of proteins or nucleic acids for biochemical studies. Moreover, they can overcome ethical concerns associated with the use of animal and human tissue and allow for fostering of the 3R principle of replacement, reduction, and refinement proposed in 1959 by William M. S. Russell and Rex L. Burch. Nevertheless, working with continuous cell lines also has some disadvantages. In particular, there are ample examples in which genetic drift and cell misidentification has led to invalid data. Therefore, many journals and granting agencies now recommend proper cell line authentication. We herein describe the genetic characterization of the rat HSC line HSC-T6, which was introduced as a new in vitro model for the study of retinoid metabolism. The consensus chromosome markers, outlined primarily through multicolor spectral karyotyping (SKY), demonstrate that apart from the large derivative chromosome 1 (RNO1), at least two additional chromosomes (RNO4 and RNO7) are found to be in three copies in all metaphases. Additionally, we have defined a short tandem repeat (STR) profile for HSC-T6, including 31 species-specific markers. The typical features of these cells have been further determined by electron microscopy, Western blotting, and Rhodamine-Phalloidin staining. Finally, we have analyzed the transcriptome of HSC-T6 cells by mRNA sequencing (mRNA-Seq) using next generation sequencing (NGS). Full article
(This article belongs to the Special Issue Cell Biology Research in Germany: State-of-the-Art and Perspectives in Cellular Pathology)
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Review

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18 pages, 1892 KiB  
Review
The Human Ntn-Hydrolase Superfamily: Structure, Functions and Perspectives
by Arne Linhorst and Torben Lübke
Cells 2022, 11(10), 1592; https://doi.org/10.3390/cells11101592 - 10 May 2022
Cited by 13 | Viewed by 2852
Abstract
N-terminal nucleophile (Ntn)-hydrolases catalyze the cleavage of amide bonds in a variety of macromolecules, including the peptide bond in proteins, the amide bond in N-linked protein glycosylation, and the amide bond linking a fatty acid to sphingosine in complex sphingolipids. Ntn-hydrolases are all [...] Read more.
N-terminal nucleophile (Ntn)-hydrolases catalyze the cleavage of amide bonds in a variety of macromolecules, including the peptide bond in proteins, the amide bond in N-linked protein glycosylation, and the amide bond linking a fatty acid to sphingosine in complex sphingolipids. Ntn-hydrolases are all sharing two common hallmarks: Firstly, the enzymes are synthesized as inactive precursors that undergo auto-proteolytic self-activation, which, as a consequence, reveals the active site nucleophile at the newly formed N-terminus. Secondly, all Ntn-hydrolases share a structural consistent αββα-fold, notwithstanding the total lack of amino acid sequence homology. In humans, five subclasses of the Ntn-superfamily have been identified so far, comprising relevant members such as the catalytic active subunits of the proteasome or a number of lysosomal hydrolases, which are often associated with lysosomal storage diseases. This review gives an updated overview on the structural, functional, and (patho-)physiological characteristics of human Ntn-hydrolases, in particular. Full article
(This article belongs to the Special Issue Cell Biology Research in Germany: State-of-the-Art and Perspectives in Cellular Pathology)
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