scholarly journals Cell Death Related Proteins Beyond Apoptosis in the CNS

2022 ◽  
Vol 9 ◽  
Author(s):  
Bazhena Bahatyrevich-Kharitonik ◽  
Rafael Medina-Guzman ◽  
Alicia Flores-Cortes ◽  
Marta García-Cruzado ◽  
Edel Kavanagh ◽  
...  
Keyword(s):  
Cell Death ◽  
Protein Function ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Original Function ◽  
New Concepts ◽  
Cytoskeleton Reorganization ◽  
Caspase Substrates ◽  
Cell Death Signaling ◽  
Related Proteins

Cell death related (CDR) proteins are a diverse group of proteins whose original function was ascribed to apoptotic cell death signaling. Recently, descriptions of non-apoptotic functions for CDR proteins have increased. In this minireview, we comment on recent studies of CDR proteins outside the field of apoptosis in the CNS, encompassing areas such as the inflammasome and non-apoptotic cell death, cytoskeleton reorganization, synaptic plasticity, mitophagy, neurodegeneration and calcium signaling among others. Furthermore, we discuss the evolution of proteomic techniques used to predict caspase substrates that could potentially explain their non-apoptotic roles. Finally, we address new concepts in the field of non-apoptotic functions of CDR proteins that require further research such the effect of sexual dimorphism on non-apoptotic CDR protein function and the emergence of zymogen-specific caspase functions.

scholarly journals FRL, a Novel Formin-Related Protein, Binds to Rac and Regulates Cell Motility and Survival of Macrophages

2000 ◽  
Vol 20 (18) ◽  
pp. 6872-6881 ◽  
Author(s):  
Shinri Yayoshi-Yamamoto ◽  
Ichiro Taniuchi ◽  
Takeshi Watanabe
Keyword(s):  
Cell Death ◽  
Cell Adhesion ◽  
Bone Marrow Cells ◽  
Apoptotic Cell ◽  
Small Gtpases ◽  
Apoptotic Cell Death ◽  
Cell Adhesion And Migration ◽  
Rho Family ◽  
And Migration ◽  
Related Proteins

ABSTRACT We have isolated a cDNA, frl(formin-related gene in leukocytes), a novel mammalian member of the formin gene family. The frlcDNA encodes a 160-kDa protein, FRL, that possesses FH1, FH2, and FH3 domains that are well conserved among other Formin-related proteins. An FRL protein is mainly localized in the cytosol and is highly expressed in spleen, lymph node, and bone marrow cells. Formin-related genes and proteins have been reported to play crucial roles in morphogenesis, cell polarity, and cytokinesis through interaction with Rho family small GTPases. FRL binds to Rac at its N-terminal region including the FH3 domain and associates with profilin at the FH1 domain. In a macrophage cell line, P388D1, overexpression of a truncated form of FRL containing only the FH3 domain (FH3-FRL) strongly inhibited cell adhesion to fibronectin and migration upon stimulation with a chemokine. Moreover, expression of the truncated FH3-FRL protein resulted in apoptotic cell death of P388D1 cells, suggesting that the truncated FH3-FRL protein may interfere with signals of FRL. Overexpression in the P388D1 cells of full-length FRL or of the truncated protein containing the FH3 and FH1 domains, with simultaneous expression of the truncated FH3-FRL protein, blocked apoptotic cell death and inhibition of cell adhesion and migration. These results suggest that FRL may play a role in the control of reorganization of the actin cytoskeleton in association with Rac and also in the regulation of the signal for cell survival.

scholarly journals Calcium and cell death signaling in neurodegeneration and aging

2009 ◽  
Vol 81 (3) ◽  
pp. 467-475 ◽  
Author(s):  
Soraya Smaili ◽  
Hanako Hirata ◽  
Rodrigo Ureshino ◽  
Priscila T. Monteforte ◽  
Ana P. Morales ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Apoptotic Cell ◽  
Essential Elements ◽  
Apoptotic Cell Death ◽  
Nuclear Fragmentation ◽  
Physiological Processes ◽  
Cell Death Signaling ◽  
Lines Of Evidence

Transient increase in cytosolic (Cac2+) and mitochondrial Ca2+ (Ca m2+) are essential elements in the control of many physiological processes. However, sustained increases in Ca c2+ and Ca m2+ may contribute to oxidative stress and cell death. Several events are related to the increase in Ca m2+, including regulation and activation of a number of Ca2+ dependent enzymes, such as phospholipases, proteases and nucleases. Mitochondria and endoplasmic reticulum (ER) play pivotal roles in the maintenance of intracellular Ca2+ homeostasis and regulation of cell death. Several lines of evidence have shown that, in the presence of some apoptotic stimuli, the activation of mitochondrial processes maylead to the release of cytochrome c followed by the activation of caspases, nuclear fragmentation and apoptotic cell death. The aim of this review was to show how changes in calcium signaling can be related to the apoptotic cell death induction. Calcium homeostasis was also shown to be an important mechanism involved in neurodegenerative and aging processes.

scholarly journals Otoprotective Effect of 2,3,4′,5-Tetrahydroxystilbene-2-O-β-d-Glucoside on Gentamicin-Induced Apoptosis in Mouse Cochlear UB/OC-2 Cells

Molecules ◽  
2020 ◽  
Vol 25 (13) ◽  
pp. 3070
Author(s):  
Yu-Hsuan Wen ◽  
Jia-Ni Lin ◽  
Rong-Shuan Wu ◽  
Szu-Hui Yu ◽  
Chuan-Jen Hsu ◽  
...  
Keyword(s):  
Cell Death ◽  
Molecular Mechanisms ◽  
Apoptotic Cell ◽  
Therapeutic Option ◽  
Apoptotic Cell Death ◽  
Ros Generation ◽  
Sod Activity ◽  
Ldh Release ◽  
Induced Apoptosis ◽  
Related Proteins

Excessive levels of reactive oxygen species (ROS) lead to mitochondrial damage and apoptotic cell death in gentamicin-induced ototoxicity. 2,3,4’,5-Tetrahydroxystilbene-2-O-β-d-glucoside (THSG), a bioactive constituent, isolated from Polygonum multiflorum Thunb., exhibits numerous biological benefits in treating aging-related diseases by suppressing oxidative damage. However, its protective effect on gentamicin-induced ototoxicity remains unexplored. Therefore, here, we aimed to investigate the otoprotective effect of THSG on gentamicin-induced apoptosis in mouse cochlear UB/OC-2 cells. We evaluated the effect of gentamicin and THSG on the ROS level, superoxide dismutase (SOD) activity, mitochondrial membrane potential, nuclear condensation, and lactate dehydrogenase (LDH) release, and the expression of apoptosis-related proteins was assessed to understand the molecular mechanisms underlying its preventive effects. The findings demonstrated that gentamicin increased ROS generation, LDH release, and promoted apoptotic cell death in UB/OC-2 cells. However, THSG treatment reversed these effects by suppressing ROS production and downregulating the mitochondrial-dependent apoptotic pathway. Additionally, it increased the SOD activity, decreased the expression of apoptosis-related proteins, alleviated the levels of the apoptotic cells, and impaired cytotoxicity. To the best of our knowledge, this is the first study to demonstrate that THSG could be a potential therapeutic option to attenuate gentamicin-induced ototoxicity.

scholarly journals Mitochondrial IF1preserves cristae structure to limit apoptotic cell death signaling

Cell Cycle ◽  
2013 ◽  
Vol 12 (16) ◽  
pp. 2530-2532 ◽  
Author(s):  
Danilo Faccenda ◽  
Choon H Tan ◽  
Michael R Duchen ◽  
Michelangelo Campanella
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Cell Death Signaling

scholarly journals Non-Apoptotic Cell Death Signaling Pathways in Melanoma

2020 ◽  
Vol 21 (8) ◽  
pp. 2980 ◽  
Author(s):  
Mariusz L. Hartman
Keyword(s):  
Cell Death ◽  
Signaling Pathways ◽  
Melanoma Cell ◽  
Apoptotic Cell ◽  
Genetic Alterations ◽  
Melanoma Cells ◽  
Apoptotic Cell Death ◽  
Specific Cell ◽  
Anti Cancer ◽  
Cell Death Signaling

Resisting cell death is a hallmark of cancer. Disturbances in the execution of cell death programs promote carcinogenesis and survival of cancer cells under unfavorable conditions, including exposition to anti-cancer therapies. Specific modalities of regulated cell death (RCD) have been classified based on different criteria, including morphological features, biochemical alterations and immunological consequences. Although melanoma cells are broadly equipped with the anti-apoptotic machinery and recurrent genetic alterations in the components of the RAS/RAF/MEK/ERK signaling markedly contribute to the pro-survival phenotype of melanoma, the roles of autophagy-dependent cell death, necroptosis, ferroptosis, pyroptosis, and parthanatos have recently gained great interest. These signaling cascades are involved in melanoma cell response and resistance to the therapeutics used in the clinic, including inhibitors of BRAFmut and MEK1/2, and immunotherapy. In addition, the relationships between sensitivity to non-apoptotic cell death routes and specific cell phenotypes have been demonstrated, suggesting that plasticity of melanoma cells can be exploited to modulate response of these cells to different cell death stimuli. In this review, the current knowledge on the non-apoptotic cell death signaling pathways in melanoma cell biology and response to anti-cancer drugs has been discussed.

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