Special Issue "2018 Select Papers by Cells’ Editorial Board Members"

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

Deadline for manuscript submissions: closed (31 December 2018).

Special Issue Editor

Dr. Alexander E. Kalyuzhny
E-Mail Website
Guest Editor
Neuroscience, UMN Twin Cities, 6-145 Jackson Hall, 321 Church St SE, Minneapolis, MN 55455, USA
Tel. +1 612 624 2991
Special Issues and Collections in MDPI journals

Special Issue Information

Dear Colleagues,

I am pleased to announce a new Special Issue that is quite different from our typical Special Issues, which have focused on either selected areas of research or special techniques. Being creative in many ways, with this issue, Cells is compiling a collection of papers submitted exclusively by its Editorial Board Members (EBMs) covering different areas of cell research including autophagy, apoptosis, nuclear membrane, etc. As the old saying goes, “a scientist is only as good as the way he writes about his science”. The main idea behind compiling such a Special Issue, titled “2018 Select Papers by Cells’ Editorial Board Members,” is to turn the tables and allow our readers to be the judges of our board members. With this Special Issue, we also want to celebrate granting Cells an impact factor (IF), which we earned by many years of hard work, dedication, and commitment from our EBMs.

Our new Special Issue can be also viewed as a way of introducing Cells’ EBMs to top-notch researchers, so they will consider our journal a first-class platform for exchanging their scientific data.

Dr. Alexander E. Kalyuzhny
Guest Editor

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 papers will be 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 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 2000 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 (4 papers)

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Research

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Open AccessArticle
Pathophysiological Alterations of Redox Signaling and Endocannabinoid System in Granulocytes and Plasma of Psoriatic Patients
Cells 2018, 7(10), 159; https://doi.org/10.3390/cells7100159 - 06 Oct 2018
Cited by 8
Abstract
Inflammatory granulocytes are characterized by an oxidative burst, which may promote oxidative stress and lipid modification both in affected tissues and on a systemic level. On the other hand, redox signaling involving lipid peroxidation products acting as second messengers of free radicals play [...] Read more.
Inflammatory granulocytes are characterized by an oxidative burst, which may promote oxidative stress and lipid modification both in affected tissues and on a systemic level. On the other hand, redox signaling involving lipid peroxidation products acting as second messengers of free radicals play important yet not fully understood roles in the pathophysiology of inflammation and various stress-associated disorders. Therefore, the aim of this study was to evaluate the onset of oxidative stress and alterations of enzyme-dependent lipid metabolism resulting from redox imbalance in granulocytes and plasma obtained from patients with psoriasis vulgaris or psoriatic arthritis in comparison to the healthy subjects. The results obtained revealed enhanced activity of pro-oxidant enzymes nicotinamide adenine dinucleotide phosphate (NADPH) and xanthine oxidases in granulocytes with a decrease of enzymatic and non-enzymatic antioxidants in the plasma of psoriatic patients. The nuclear factor erythroid 2–related factor 2 (Nrf2) and its regulators were increased in both forms of psoriasis while heme oxygenase 1 levels were increased only in psoriasis vulgaris. The redox imbalance was associated with decreased levels of phospholipids and of free polyunsaturated fatty acids but with enhanced activity of enzymes involved in lipid metabolism (phospholipase A2, acetylhydrolase PAF, cyclooxygenases 1 and 2) and increased lipid peroxidation products 4-hydroxynonenal, isoprostanes, and neuroprostanes. Increased endocannabinoids and G protein-coupled receptor 55 were observed in both forms of the disease while expression of the cannabinoid type 1 receptor (CB1) was increased only in patients with psoriatic arthritis, which is opposite to the cannabinoid type 2 receptor. This receptor was increased only in psoriasis vulgaris. Changes in protein expression promoted the apoptosis of granulocytes by increased caspases mainly in psoriasis vulgaris. This study indicates that inhibition of the Nrf2 pathway in psoriatic arthritis promotes a redox imbalance. In addition, increased expression of CB1 receptors leads to increased oxidative stress, lipid modifications, and inflammation, which, in turn, may promote the progression of psoriasis into the advanced, arthritic form of the disease. Full article
(This article belongs to the Special Issue 2018 Select Papers by Cells’ Editorial Board Members)
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Review

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Open AccessReview
mTOR: A Cellular Regulator Interface in Health and Disease
Cells 2019, 8(1), 18; https://doi.org/10.3390/cells8010018 - 02 Jan 2019
Cited by 22
Abstract
The mechanistic target of Rapamycin (mTOR) is a ubiquitously-conserved serine/threonine kinase, which has a central function in integrating growth signals and orchestrating their physiologic effects on cellular level. mTOR is the core component of differently composed signaling complexes that differ in protein composition [...] Read more.
The mechanistic target of Rapamycin (mTOR) is a ubiquitously-conserved serine/threonine kinase, which has a central function in integrating growth signals and orchestrating their physiologic effects on cellular level. mTOR is the core component of differently composed signaling complexes that differ in protein composition and molecular targets. Newly identified classes of mTOR inhibitors are being developed to block autoimmune diseases and transplant rejections but also to treat obesity, diabetes, and different types of cancer. Therefore, the selective and context-dependent inhibition of mTOR activity itself might come into the focus as molecular target to prevent severe diseases and possibly to extend life span. This review provides a general introduction to the molecular composition and physiologic function of mTOR complexes as part of the Special Issue “2018 Select Papers by Cells’ Editorial Board Members”. Full article
(This article belongs to the Special Issue 2018 Select Papers by Cells’ Editorial Board Members)
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Open AccessFeature PaperReview
Vitamin B6 and Its Role in Cell Metabolism and Physiology
Cells 2018, 7(7), 84; https://doi.org/10.3390/cells7070084 - 22 Jul 2018
Cited by 23
Abstract
Vitamin B6 is one of the most central molecules in cells of living organisms. It is a critical co-factor for a diverse range of biochemical reactions that regulate basic cellular metabolism, which impact overall physiology. In the last several years, major progress [...] Read more.
Vitamin B6 is one of the most central molecules in cells of living organisms. It is a critical co-factor for a diverse range of biochemical reactions that regulate basic cellular metabolism, which impact overall physiology. In the last several years, major progress has been accomplished on various aspects of vitamin B6 biology. Consequently, this review goes beyond the classical role of vitamin B6 as a cofactor to highlight new structural and regulatory information that further defines how the vitamin is synthesized and controlled in the cell. We also discuss broader applications of the vitamin related to human health, pathogen resistance, and abiotic stress tolerance. Overall, the information assembled shall provide helpful insight on top of what is currently known about the vitamin, along with addressing currently open questions in the field to highlight possible approaches vitamin B6 research may take in the future. Full article
(This article belongs to the Special Issue 2018 Select Papers by Cells’ Editorial Board Members)
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Other

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Open AccessCommentary
Perturbations in Traffic: Aberrant Nucleocytoplasmic Transport at the Heart of Neurodegeneration
Cells 2018, 7(12), 232; https://doi.org/10.3390/cells7120232 - 26 Nov 2018
Cited by 6
Abstract
Neurodegenerative diseases, such as amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and Huntington’s disease (HD), are characterized by intracellular aggregation of proteins. In the case of ALS and FTD, these protein aggregates are found in the cytoplasm of affected neurons and contain certain [...] Read more.
Neurodegenerative diseases, such as amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and Huntington’s disease (HD), are characterized by intracellular aggregation of proteins. In the case of ALS and FTD, these protein aggregates are found in the cytoplasm of affected neurons and contain certain RNA-binding proteins (RBPs), namely the TAR DNA-binding protein of 43 kDa (TDP-43) and the fused in sarcoma (FUS) gene product. TDP-43 and FUS are nuclear proteins and their displacement to the cytoplasm is thought to be adverse in at least two ways: loss-of-function in the nucleus and gain-of-toxicity in the cytoplasm. In the case of HD, expansion of a polyglutamine (polyQ) stretch within the N-terminal domain of the Huntingtin (HTT) protein leads to nuclear accumulation of polyQ HTT (or mHTT) and a toxic gain-of-function phenotype resulting in neurodegeneration. Numerous studies in recent years have provided evidence that defects in nucleocytoplasmic transport critically contribute to the pathology of these neurodegenerative diseases. A new mechanistic view is emerging, implicating three types of perturbations in normal cellular pathways that rely on nucleocytoplasmic transport: displacement of nuclear transport receptors and nucleoporins from nuclear pore complexes (NPCs), mislocalization and aggregation of RNA-binding proteins, and weakening of the chaperone activity of nuclear import receptors. Full article
(This article belongs to the Special Issue 2018 Select Papers by Cells’ Editorial Board Members)
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