scholarly journals Role of Platelet-Activating Factor in Cell Death Signaling in the Cornea: A Review

2010 ◽  
Vol 42 (1) ◽  
pp. 32-38 ◽  
Author(s):  
Salomon Esquenazi ◽  
Haydee E. P. Bazan
Keyword(s):  
Cell Death ◽  
Platelet Activating Factor ◽  
Cell Death Signaling

scholarly journals Proapoptotic Bad Involved in Brain Development, When Severely Defected, Induces Dramatic Malformation in Zebrafish

2021 ◽  
Vol 22 (9) ◽  
pp. 4832
Author(s):  
Jo-Chi Hung ◽  
Jen-Leih Wu ◽  
Jiann-Ruey Hong
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Environmental Stress ◽  
Brain Development ◽  
The Novel ◽  
Germ Layers ◽  
Cell Death Signaling ◽  
Morpholino Oligonucleotides ◽  
Material Factor

The BH3-only molecule Bad regulates cell death via its differential protein phosphorylation, but very few studies address its effect on early embryonic development in vertebrate systems. In this work, we examined the novel role of zebrafish Bad in the initial programmed cell death (PCD) for brain morphogenesis through reducing environmental stress and cell death signaling. Bad was considered to be a material factor that because of the knockdown of Bad by morpholino oligonucleotides, PCD was increased and the reactive oxygen species (ROS) level was enhanced, which correlated to trigger a p53/caspase-8 involving cell death signaling. This Bad knockdown-mediated environmental stress and enhanced cell dying can delay normal cell migration in the formation of the three germ layers, especially the ectoderm, for further brain development. Furthermore, Bad defects involved in three-germ-layers development at 8 hpf were identified by in situ hybridization approach on cyp26, rtla, and Sox17 pattern expression markers. Finally, the Bad knockdown-induced severely defected brain was examined by tissue section from 24 to 48 h postfertilization (hpf), which correlated to induce dramatic malformation in the hindbrain. Our data suggest that the BH3-only molecule Bad regulates brain development via controlling programmed cell death on overcoming environmental stress for reducing secondary cell death signaling, which suggests that correlates to brain developmental and neurological disorders in this model system.

scholarly journals Antioxidants Targeting Mitochondrial Oxidative Stress: Promising Neuroprotectants for Epilepsy

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Nan Yang ◽  
Qi-Wen Guan ◽  
Fang-Hui Chen ◽  
Qin-Xuan Xia ◽  
Xi-Xi Yin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Brain Activity ◽  
Related Factor ◽  
Mitochondrial Oxidative Stress ◽  
Electrical Brain Activity ◽  
Neuroprotective Strategies ◽  
Cell Death Signaling ◽  
Stress Oxidative

Mitochondria are major sources of reactive oxygen species (ROS) within the cell and are especially vulnerable to oxidative stress. Oxidative damage to mitochondria results in disrupted mitochondrial function and cell death signaling, finally triggering diverse pathologies such as epilepsy, a common neurological disease characterized with aberrant electrical brain activity. Antioxidants are considered as promising neuroprotective strategies for epileptic condition via combating the deleterious effects of excessive ROS production in mitochondria. In this review, we provide a brief discussion of the role of mitochondrial oxidative stress in the pathophysiology of epilepsy and evidences that support neuroprotective roles of antioxidants targeting mitochondrial oxidative stress including mitochondria-targeted antioxidants, polyphenols, vitamins, thiols, and nuclear factor E2-related factor 2 (Nrf2) activators in epilepsy. We point out these antioxidative compounds as effectively protective approaches for improving prognosis. In addition, we specially propose that these antioxidants exert neuroprotection against epileptic impairment possibly by modulating cell death interactions, notably autophagy-apoptosis, and autophagy-ferroptosis crosstalk.

Cadmium toxicity in cultured tomato cells-Role of ethylene, proteases and oxidative stress in cell death signaling

2008 ◽  
Vol 32 (12) ◽  
pp. 1521-1529 ◽  
Author(s):  
Elena T. Iakimova ◽  
Ernst J. Woltering ◽  
Veneta M. Kapchina-Toteva ◽  
Frans J.M. Harren ◽  
Simona M. Cristescu
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Cadmium Toxicity ◽  
Cell Death Signaling ◽  
And Oxidative Stress

scholarly journals A coevolved EDS1-SAG101-NRG1 module mediates cell death signaling by TIR-domain immune receptors

2019 ◽  
Author(s):  
Dmitry Lapin ◽  
Viera Kovacova ◽  
Xinhua Sun ◽  
Joram Dongus ◽  
Deepak D. Bhandari ◽  
...  
Keyword(s):  
Cell Death ◽  
Coiled Coil ◽  
Rate Variation ◽  
Distinctive Features ◽  
Tir Domain ◽  
Immune Receptors ◽  
Pathogen Effectors ◽  
Cell Death Signaling ◽  
Basal Defense

AbstractPlant intracellular nucleotide-binding/leucine-rich repeat (NLR) immune receptors are activated by pathogen effectors to trigger host defenses and cell death. Toll-Interleukin1-receptor (TIR)-domain NLRs (TNLs) converge on the Enhanced Disease Susceptibility1 (EDS1) family of lipase-like proteins for all resistance outputs. In Arabidopsis TNL immunity,AtEDS1 heterodimers with Phytoalexin Deficient4 (AtPAD4) transcriptionally boost basal defense pathways.AtEDS1 uses the same surface to interact with PAD4-related Senescence-Associated Gene101 (AtSAG101), but the role ofAtEDS1-AtSAG101 heterodimers was unclear. We show thatAtEDS1-AtSAG101 function together withAtNRG1 coiled-coil domain helper NLRs as a coevolved TNL cell death signaling module.AtEDS1-AtSAG101-AtNRG1 cell death activity is transferable to the solanaceous species,Nicotiana benthamiana, and cannot be substituted byAtEDS1-AtPAD4 withAtNRG1 orAtEDS1-AtSAG101 with endogenousNbNRG1. Analysis of EDS1-family evolutionary rate variation and heterodimer structure-guided phenotyping ofAtEDS1 variants orAtPAD4-AtSAG101 chimeras identify closely aligned α-helical coil surfaces in theAtEDS1-AtSAG101 partner C-terminal domains that are necessary for TNL cell death signaling. Our data suggest that TNL-triggered cell death and pathogen growth restriction are determined by distinctive features of EDS1-SAG101 and EDS1-PAD4 complexes and that these signaling machineries coevolved with further components within plant species or clades to regulate downstream pathways in TNL immunity.

Exploring the Role of Phytochemicals as Potent Natural Photosensitizers in Photodynamic Therapy

2020 ◽  
Vol 20 (15) ◽  
pp. 1831-1844 ◽  
Author(s):  
Giftson J. Senapathy ◽  
Blassan P. George ◽  
Heidi Abrahamse
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Cancer Treatments ◽  
Cancer Cell Death ◽  
Clinical Investigations ◽  
Cell Death Signaling ◽  
Deadly Disease ◽  
Treatment Procedures ◽  
Apoptosis And Necrosis

Background: Cancer is still considered a deadly disease worldwide due to difficulties in diagnosis, painful treatment procedures, costly therapies, side effects, and cancer relapse. Cancer treatments using conventional methods like chemotherapy and radiotherapy were not convincing due to its post-treatment toxicity in the host. In Photodynamic Therapy (PDT), three individual non-toxic components including a photosensitizer, light source and oxygen cause damage to the cells and tissues when they are combined. Objective: In recent years, phytochemicals are being increasingly recognized as potent complementary drugs for cancer because of its natural availability, less toxicity and therapeutic efficiency in par with commercial drugs. Hence, the idea of using phytochemicals as natural photosensitizers in PDT resulted in a multiple pool of research studies with promising results in preclinical and clinical investigations. Methods: In this review, the potential of phytochemicals to act as natural photosensitizers for PDT, their mode of action, drawbacks, challenges and possible solutions are discussed in detail. Results: In PDT, natural photosensitizers, when used alone or in combination with other photosensitizers, induced cell death by apoptosis and necrosis, increased oxidative stress, altered cancer cell death signaling pathways, increased cytotoxicity and DNA damage in cancer cells. The pro-oxidant nature of certain antioxidant polyphenols, hormesis phenomenon, Warburg effect and DNA damaging potential plays a significant role in the photosensitizing mechanism of phytochemicals in PDT. Conclusion: This review explores the role of phytochemicals that can act as photosensitizers alone or in combination with PDT and its mechanism of action on different cancers.

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