scholarly journals The role of death domain proteins in host response upon SARS-CoV-2 infection: modulation of programmed cell death and translational applications

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Nikita V. Ivanisenko ◽  
Kamil Seyrek ◽  
Nikolay A. Kolchanov ◽  
Vladimir A. Ivanisenko ◽  
Inna N. Lavrik
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Molecular Mechanisms ◽  
Control Cell ◽  
Death Domain ◽  
Global Public Health ◽  
Cell Death Pathways ◽  
Rapid Spread ◽  
Cell Signaling Networks

Abstract The current pandemic of novel severe acute respiratory syndrome coronavirus (SARS-CoV-2) poses a significant global public health threat. While urgent regulatory measures in control of the rapid spread of this virus are essential, scientists around the world have quickly engaged in this battle by studying the molecular mechanisms and searching for effective therapeutic strategies against this deadly disease. At present, the exact mechanisms of programmed cell death upon SARS-CoV-2 infection remain to be elucidated, though there is increasing evidence suggesting that cell death pathways play a key role in SARS-CoV-2 infection. There are several types of programmed cell death, including apoptosis, pyroptosis, and necroptosis. These distinct programs are largely controlled by the proteins of the death domain (DD) superfamily, which play an important role in viral pathogenesis and host antiviral response. Many viruses have acquired the capability to subvert the program of cell death and evade the host immune response, mainly by virally encoded gene products that control cell signaling networks. In this mini-review, we will focus on SARS-CoV-2, and discuss the implication of restraining the DD-mediated signaling network to potentially suppress viral replication and reduce tissue damage.

scholarly journals An Endopolygalacturonase from Sclerotinia sclerotiorum Induces Calcium-Mediated Signaling and Programmed Cell Death in Soybean Cells

2005 ◽  
Vol 18 (8) ◽  
pp. 849-855 ◽  
Author(s):  
Anna Zuppini ◽  
Lorella Navazio ◽  
Luca Sella ◽  
Carala Castiglioni ◽  
Francesco Favaron ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Sclerotinia Sclerotiorum ◽  
Phase 1 ◽  
Control Cell ◽  
Cell Contact ◽  
Cytochrome C Release ◽  
Soybean Seedlings ◽  
Polygalacturonase Inhibiting Protein

A basic endopolygalacturonase (PG) isoform, produced early by Sclerotinia sclerotiorum when infecting soybean seedlings, was used to examine the signaling role of the enzyme in aequorin-expressing soybean cells. A cytosolic Ca2+ elevation was induced, with a rapid increase (phase 1) and a very slow decrease (phase 2) of Ca2+ concentration, indicating the involvement of Ca2+ ions in PG signaling. Within 1 h of PG-cell contact a remarkable level of cell death was recorded, significantly higher than the control cell culture turnover. The observed morphological and biochemical changes were indicative of the activation of programmed cell death; in particular, cytochrome c release in the cytoplasm and activation of both caspase 9-like and caspase 3-like proteases were found. When a polygalacturonase-inhibiting protein (PGIP) and the PG were simultaneously applied to cells, both the Ca2+ increase and cell death were annulled. The possible roles of prolonged sustained cytosolic Ca2+ concentrations in inducing cell death and of the PG-PGIP interaction in preventing PG signaling are discussed.

scholarly journals Programmed Cell Death in the Small Intestine: Implications for the Pathogenesis of Celiac Disease

2021 ◽  
Vol 22 (14) ◽  
pp. 7426
Author(s):  
Federico Perez ◽  
Carolina Nayme Ruera ◽  
Emanuel Miculan ◽  
Paula Carasi ◽  
Fernando Gabriel Chirdo
Keyword(s):  
Cell Death ◽  
Small Intestine ◽  
Celiac Disease ◽  
Programmed Cell Death ◽  
Oral Tolerance ◽  
Recent Literature ◽  
High Rate ◽  
Inflammatory Pathways ◽  
Cell Death Pathways

The small intestine has a high rate of cell turnover under homeostatic conditions, and this increases further in response to infection or damage. Epithelial cells mostly die by apoptosis, but recent studies indicate that this may also involve pro-inflammatory pathways of programmed cell death, such as pyroptosis and necroptosis. Celiac disease (CD), the most prevalent immune-based enteropathy, is caused by loss of oral tolerance to peptides derived from wheat, rye, and barley in genetically predisposed individuals. Although cytotoxic cells and gluten-specific CD4+ Th1 cells are the central players in the pathology, inflammatory pathways induced by cell death may participate in driving and sustaining the disease through the release of alarmins. In this review, we summarize the recent literature addressing the role of programmed cell death pathways in the small intestine, describing how these mechanisms may contribute to CD and discussing their potential implications.

Regulation of necroptosis signaling and cell death by reactive oxygen species

2016 ◽  
Vol 397 (7) ◽  
pp. 657-660 ◽  
Author(s):  
Simone Fulda
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Signaling Pathways ◽  
Posttranslational Modifications ◽  
Molecular Mechanisms ◽  
Reactive Oxygen ◽  
Alternative Form ◽  
Oxygen Species

Abstract Necroptosis has recently been identified as an alternative form of programmed cell death that is characterized by defined molecular mechanisms. Reactive oxygen species (ROS) are involved in the regulation of numerous signaling pathways, as they are highly reactive and can cause (ir)reversible posttranslational modifications. While the role of ROS in other modes of cell death has been extensively studied, its impact on necroptotic signaling and cell death is far less clear. The current minireview discusses the evidence for and against a role of ROS in necroptosis.

scholarly journals Fungal-Induced Programmed Cell Death

2021 ◽  
Vol 7 (3) ◽  
pp. 231
Author(s):  
Thomas J. Williams ◽  
Luis E. Gonzales-Huerta ◽  
Darius Armstrong-James
Keyword(s):  
Immune Response ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Opportunistic Infections ◽  
Fungal Infections ◽  
Pathogenic Fungi ◽  
Fungal Pathogenicity ◽  
Cell Death Pathways ◽  
Fungal Immunity

Fungal infections are a cause of morbidity in humans, and despite the availability of a range of antifungal treatments, the mortality rate remains unacceptably high. Although our knowledge of the interactions between pathogenic fungi and the host continues to grow, further research is still required to fully understand the mechanism underpinning fungal pathogenicity, which may provide new insights for the treatment of fungal disease. There is great interest regarding how microbes induce programmed cell death and what this means in terms of the immune response and resolution of infection as well as microbe-specific mechanisms that influence cell death pathways to aid in their survival and continued infection. Here, we discuss how programmed cell death is induced by fungi that commonly cause opportunistic infections, including Candida albicans, Aspergillus fumigatus, and Cryptococcus neoformans, the role of programmed cell death in fungal immunity, and how fungi manipulate these pathways.

scholarly journals Adaptive Role of Cell Death in Yeast Communities Stressed with Macrolide Antifungals

mSphere ◽  
2021 ◽  
Author(s):  
N. A. Kireeva ◽  
S. S. Sokolov ◽  
E. A. Smirnova ◽  
K. V. Galkina ◽  
F. F. Severin ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Molecular Mechanisms ◽  
Eukaryotic Microorganisms ◽  
Adaptive Role

Eukaryotic microorganisms harbor elements of programmed cell death (PCD) mechanisms that are homologous to the PCD of multicellular metazoa. However, it is still debated whether microbial PCD has an adaptive role or whether the processes of cell death are an aimless operation in self-regulating molecular mechanisms.

scholarly journals Programmed Cell Death Pathways in the Pathogenesis of Systemic Lupus Erythematosus

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Fangyuan Yang ◽  
Yi He ◽  
Zeqing Zhai ◽  
Erwei Sun
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Immune Responses ◽  
Lupus Erythematosus ◽  
Tissue Damage ◽  
Systemic Lupus ◽  
Secondary Necrosis ◽  
Cell Death Pathways

Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease characterized by excessive inflammatory and immune responses and tissue damage. Increasing evidence has demonstrated the important role of programmed cell death in SLE pathogenesis. When apoptosis encounters with defective clearance, accumulated apoptotic cells lead to secondary necrosis. Different forms of lytic cell death, including secondary necrosis after apoptosis, NETosis, necroptosis, and pyroptosis, contribute to the release of damage-associated molecular patterns (DAMPs) and autoantigens, resulting in triggering immunity and tissue damage in SLE. However, the role of autophagy in SLE pathogenesis is in dispute. This review briefly discusses different forms of programmed cell death pathways and lay particular emphasis on inflammatory cell death pathways such as NETosis, pyroptosis, and necroptosis and their roles in the inflammatory and immune responses in SLE.

scholarly journals Programmed Cell Death in SARS-CoV-2 Infection: A Short Review

2021 ◽  
Vol 1 (4) ◽  
pp. 223-228
Author(s):  
Rushikesh Deshpande ◽  
Chunbin Zou
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Short Review ◽  
Health Concern ◽  
Cell Death Pathways ◽  
Global Pandemic ◽  
Distinct Cell ◽  
Induced Apoptosis ◽  
Underlying Pathophysiology

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the latest variant in the coronavirus family, causing COVID-19, has resulted in global pandemic since early 2020 leading to severe public health concern. So far, the pandemic has caused more than 200 million infections and 4 million deaths worldwide. Most of the studies are focused on developing prevention, intervention, and therapeutic strategies. However, underlying pathophysiology of the disease is important as well, which needs further attention. Cell death is one of the major causative mechanisms that leads to severe inflammation, and it is also an a posteriori consequence of the hyperinflammatory storm that renders poor prognosis of the disease. Substantial cell death has been reported in biopsy samples from post mortem patients. Among the distinct cell death pathways, apoptosis, the regulated programmed cell death plays an important role in the pathogenesis of the disease. Understanding the role of SARS-CoV-2 infection in apoptosis is critical to linearize the pathogenesis of the virus as well as the resultant disease, that may uncover novel therapeutic targets in treatment of COVID-19 patients. Here, we review the current progress on the underlying molecular mechanism(s) of SARS-CoV-2-induced apoptosis, not only at the level of the virus but also at its individual proteins.

Sign in / Sign up

Export Citation Format

Share Document