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Stress Signaling and Programmed Cell Death 2.0
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Stress Signaling and Programmed Cell Death 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: 30 May 2024 | Viewed by 4936

Special Issue Editor

Dr. Takuya Noguchi

E-Mail Website
Guest Editor
Department of Biopharmaceutical Science, Tohoku University, Sendai 980-8578, Japan
Interests: apoptosis; signaling pathways; phosphorylation; signal transduction; cell signaling; reactive oxygen species; molecular cell biology; cell biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of our previous successful Special Issue “Stress Signaling and Programmed Cell Death”.

Organisms are continuously exposed to various types of stress from external and internal environments. In order to protect cells against such stresses, each cell is equipped with multiple signal transduction systems that elicit a wide range of cellular responses to adapt to or resist such stresses. These signal transduction systems are often described as “stress signaling”. Compelling evidence indicates that the dysregulation of stress signaling induces aberrant responses to stresses, and is responsible for various diseases. Programmed cell death (PCD) is perceived as a crucial event during development and tissue formation. As a stress response, PCD also plays a critical role in the elimination of cells suffering severe stress-induced damage to maintain homeostasis within multicellular organisms, and a number of stress signaling pathways are involved in the regulation of PCD. For this Special Issue, studies of novel signaling mechanisms and pathological processes associated with PCD are welcomed.

Dr. Takuya Noguchi
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 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • apoptosis
  • non-apoptotic cell death
  • inflammatory cell death
  • cancer
  • neurodegenerative disease.

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Published Papers (5 papers)

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Research

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28 pages, 8957 KiB  
Article
The Role of Hydrogen Sulfide in the Localization and Expression of p53 and Cell Death in the Nervous Tissue in Traumatic Brain Injury and Axotomy
by Stanislav Rodkin, Chizaram Nwosu, Margarita Raevskaya, Maxim Khanukaev, Khava Bekova, Inna Vasilieva, Diana Vishnyak, Anastasia Tolmacheva, Elena Efremova, Mitkhat Gasanov and Anton Tyurin
Int. J. Mol. Sci. 2023, 24(21), 15708; https://doi.org/10.3390/ijms242115708 - 28 Oct 2023
Viewed by 1188
Abstract
Traumatic brain injury (TBI) is one of the leading causes of disability and death worldwide. It is characterized by various molecular–cellular events, with the main ones being apoptosis and damage to axons. To date, there are no clinically effective neuroprotective drugs. In this [...] Read more.
Traumatic brain injury (TBI) is one of the leading causes of disability and death worldwide. It is characterized by various molecular–cellular events, with the main ones being apoptosis and damage to axons. To date, there are no clinically effective neuroprotective drugs. In this study, we examined the role of hydrogen sulfide (H2S) in the localization and expression of the key pro-apoptotic protein p53, as well as cell death in the nervous tissue in TBI and axotomy. We used a fast donor (sodium sulphide, Na2S) H2S and a classic inhibitor (aminooxyacetic acid, AOAA) of cystathionine β-synthase (CBS), which is a key enzyme in H2S synthesis. These studies were carried out on three models of neurotrauma in vertebrates and invertebrates. As a result, it was found that Na2S exhibits a pronounced neuroprotective effect that reduces the number of TUNEL-positive neurons and glial cells in TBI and apoptotic glia in axotomy. This effect could be realized through the Na2S-dependent decrease in the level of p53 in the cells of the nervous tissue of vertebrates and invertebrates, which we observed in our study. We also observed the opposite effect when using AOAA, which indicates the important role of CBS in the regulation of p53 expression and death of neurons and glial cells in TBI and axotomy. Full article
(This article belongs to the Special Issue Stress Signaling and Programmed Cell Death 2.0)
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13 pages, 1892 KiB  
Article
Murine Mast Cells That Are Deficient in IFNAR-Signaling Respond to Viral Infection by Producing a Large Amount of Inflammatory Cytokines, a Low Level of Reactive Oxygen Species, and a High Rate of Cell Death
by Yeganeh Mehrani, Jason P. Knapp, Julia E. Kakish, Sophie Tieu, Helia Javadi, Lily Chan, Ashley A. Stegelmeier, Christina Napoleoni, Byram W. Bridle and Khalil Karimi
Int. J. Mol. Sci. 2023, 24(18), 14141; https://doi.org/10.3390/ijms241814141 - 15 Sep 2023
Viewed by 820
Abstract
Mat cells (MCs) are located in the skin and mucous membranes at points where the body meets the environment. When activated, MCs release inflammatory cytokines, which help the immune system to fight viruses. MCs produce, and have receptors for interferons (IFNs), which belong [...] Read more.
Mat cells (MCs) are located in the skin and mucous membranes at points where the body meets the environment. When activated, MCs release inflammatory cytokines, which help the immune system to fight viruses. MCs produce, and have receptors for interferons (IFNs), which belong to a family of cytokines recognized for their antiviral properties. Previously, we reported that MCs produced proinflammatory cytokines in response to a recombinant vesicular stomatitis virus (rVSVΔm51) and that IFNAR signaling was required to down-modulate these responses. Here, we have demonstrated that UV-irradiated rVSVΔm51 did not cause any inflammatory cytokines in either in vitro cultured mouse IFNAR-intact (IFNAR+/+), or in IFNAR-knockout (IFNAR−/−) MCs. However, the non-irradiated virus was able to replicate more effectively in IFNAR−/− MCs and produced a higher level of inflammatory cytokines compared with the IFNAR+/+ MCs. Interestingly, MCs lacking IFNAR expression displayed reduced levels of reactive oxygen species (ROS) compared with IFNAR+/+ MCs. Additionally, upon the viral infection, these IFNAR−/− MCs were found to coexist with many dying cells within the cell population. Based on our findings, IFNAR-intact MCs exhibit a lower rate of rVSVΔm51 infectivity and lower levels of cytokines while demonstrating higher levels of ROS. This suggests that MCs with intact IFNAR signaling may survive viral infections by producing cell-protective ROS mechanisms and are less likely to die than IFNAR−/− cells. Full article
(This article belongs to the Special Issue Stress Signaling and Programmed Cell Death 2.0)
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20 pages, 4697 KiB  
Article
Involvement of Both Extrinsic and Intrinsic Apoptotic Pathways in Tridecylpyrrolidine-Diol Derivative-Induced Apoptosis In Vitro
by Natalia Nosalova, Alexandra Keselakova, Martin Kello, Miroslava Martinkova, Dominika Fabianova and Martina Bago Pilatova
Int. J. Mol. Sci. 2023, 24(14), 11696; https://doi.org/10.3390/ijms241411696 - 20 Jul 2023
Cited by 1 | Viewed by 1203
Abstract
Despite the decreasing trend in mortality from colorectal cancer, this disease still remains the third most common cause of death from cancer. In the present study, we investigated the antiproliferative and pro-apoptotic effects of (2S,3S,4R)-2-tridecylpyrrolidine-3,4-diol hydrochloride on [...] Read more.
Despite the decreasing trend in mortality from colorectal cancer, this disease still remains the third most common cause of death from cancer. In the present study, we investigated the antiproliferative and pro-apoptotic effects of (2S,3S,4R)-2-tridecylpyrrolidine-3,4-diol hydrochloride on colon cancer cells (Caco-2 and HCT116). The antiproliferative effect and IC50 values were determined by the MTT and BrdU assays. Flow cytometry, qRT-PCR and Western blot were used to study the cellular and molecular mechanisms involved in the induction of apoptotic pathways. Colon cancer cell migration was monitored by the scratch assay. Concentration-dependent cytotoxic and antiproliferative effects on both cell lines, with IC50 values of 3.2 ± 0.1 μmol/L (MTT) vs. 6.46 ± 2.84 μmol/L (BrdU) for HCT116 and 2.17 ± 1.5 μmol/L (MTT) vs. 1.59 ± 0.72 μmol/L (BrdU), for Caco-2 were observed. The results showed that tridecylpyrrolidine-induced apoptosis was associated with the externalization of phosphatidylserine, reduced mitochondrial membrane potential (MMP) accompanied by the activation of casp-3/7, the cleavage of PARP and casp-8, the overexpression of TNF-α and FasL and the dysregulation of Bcl-2 family proteins. Inhibition of the migration of treated cells across the wound area was detected. Taken together, our data show that the anticancer effects of tridecylpyrrolidine analogues in colon cancer cells are mediated by antiproliferative activity, the induction of both extrinsic and intrinsic apoptotic pathways and the inhibition of cell migration. Full article
(This article belongs to the Special Issue Stress Signaling and Programmed Cell Death 2.0)
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Review

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21 pages, 2446 KiB  
Review
The Intricate Balance between Life and Death: ROS, Cathepsins, and Their Interplay in Cell Death and Autophagy
by Maya V. Voronina, Anastasia S. Frolova, Ekaterina P. Kolesova, Nikita A. Kuldyushev, Alessandro Parodi and Andrey A. Zamyatnin, Jr.
Int. J. Mol. Sci. 2024, 25(7), 4087; https://doi.org/10.3390/ijms25074087 - 06 Apr 2024
Viewed by 504
Abstract
Cellular survival hinges on a delicate balance between accumulating damages and repair mechanisms. In this intricate equilibrium, oxidants, currently considered physiological molecules, can compromise vital cellular components, ultimately triggering cell death. On the other hand, cells possess countermeasures, such as autophagy, which degrades [...] Read more.
Cellular survival hinges on a delicate balance between accumulating damages and repair mechanisms. In this intricate equilibrium, oxidants, currently considered physiological molecules, can compromise vital cellular components, ultimately triggering cell death. On the other hand, cells possess countermeasures, such as autophagy, which degrades and recycles damaged molecules and organelles, restoring homeostasis. Lysosomes and their enzymatic arsenal, including cathepsins, play critical roles in this balance, influencing the cell’s fate toward either apoptosis and other mechanisms of regulated cell death or autophagy. However, the interplay between reactive oxygen species (ROS) and cathepsins in these life-or-death pathways transcends a simple cause-and-effect relationship. These elements directly and indirectly influence each other’s activities, creating a complex web of interactions. This review delves into the inner workings of regulated cell death and autophagy, highlighting the pivotal role of ROS and cathepsins in these pathways and their intricate interplay. Full article
(This article belongs to the Special Issue Stress Signaling and Programmed Cell Death 2.0)
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26 pages, 1661 KiB  
Review
An Overview of the Epigenetic Modifications in the Brain under Normal and Pathological Conditions
by Laura Lossi, Claudia Castagna and Adalberto Merighi
Int. J. Mol. Sci. 2024, 25(7), 3881; https://doi.org/10.3390/ijms25073881 - 30 Mar 2024
Viewed by 627
Abstract
Epigenetic changes are changes in gene expression that do not involve alterations to the DNA sequence. These changes lead to establishing a so-called epigenetic code that dictates which and when genes are activated, thus orchestrating gene regulation and playing a central role in [...] Read more.
Epigenetic changes are changes in gene expression that do not involve alterations to the DNA sequence. These changes lead to establishing a so-called epigenetic code that dictates which and when genes are activated, thus orchestrating gene regulation and playing a central role in development, health, and disease. The brain, being mostly formed by cells that do not undergo a renewal process throughout life, is highly prone to the risk of alterations leading to neuronal death and neurodegenerative disorders, mainly at a late age. Here, we review the main epigenetic modifications that have been described in the brain, with particular attention on those related to the onset of developmental anomalies or neurodegenerative conditions and/or occurring in old age. DNA methylation and several types of histone modifications (acetylation, methylation, phosphorylation, ubiquitination, sumoylation, lactylation, and crotonylation) are major players in these processes. They are directly or indirectly involved in the onset of neurodegeneration in Alzheimer’s or Parkinson’s disease. Therefore, this review briefly describes the roles of these epigenetic changes in the mechanisms of brain development, maturation, and aging and some of the most important factors dynamically regulating or contributing to these changes, such as oxidative stress, inflammation, and mitochondrial dysfunction. Full article
(This article belongs to the Special Issue Stress Signaling and Programmed Cell Death 2.0)
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