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Special Issue "Stress Signaling and Programmed Cell Death 2.0"

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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

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Research

Open AccessArticle

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

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

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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 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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Open AccessArticle

Involvement of Both Extrinsic and Intrinsic Apoptotic Pathways in Tridecylpyrrolidine-Diol Derivative-Induced Apoptosis In Vitro

and

Martina Bago Pilatova

Int. J. Mol. Sci. 2023, 24(14), 11696; https://doi.org/10.3390/ijms241411696 - 20 Jul 2023

Viewed by 545

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 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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