scholarly journals Dual role of poly(ADP‐ribose) glycohydrolase in the regulation of cell death in oxidatively stressed A549 cells

2009 ◽  
Vol 23 (10) ◽  
pp. 3553-3563 ◽  
Author(s):  
Katalin Erdélyi ◽  
Péter Bai ◽  
István Kovács ◽  
Éva Szabó ◽  
Gábor Mocsár ◽  
...  
Keyword(s):  
Cell Death ◽  
A549 Cells ◽  
Dual Role

scholarly journals Polymerase Acidic Subunit of H9N2 Polymerase Complex Induces Cell Apoptosis by Binding to PDCD 7 in A549 Cells

2020 ◽  
Author(s):  
Shaohua Wang ◽  
Na Li ◽  
Shugang Jin ◽  
Ruihua Zhang ◽  
Tong Xu
Keyword(s):  
Cell Death ◽  
Influenza Virus ◽  
Cell Apoptosis ◽  
Influenza A ◽  
A549 Cells ◽  
Influenza Virus Infection ◽  
Economic Loss ◽  
Poultry Production ◽  
H9n2 Influenza Virus

Abstract Background: H9N2 influenza virus, a subtype of influenza A virus, can spread across different species and induce the respiratory infectious disease in humans, leading to a severe public health risk and a huge economic loss to poultry production. Increasing studies have shown that polymerase acidic (PA) subunit of RNA polymerase in ribonucleoproteins complex of H9N2 involves in crossing the host species barriers, the replication and airborne transmission of H9N2.Methods: Here, to further investigate the role of PA subunit during the infection of H9N2 influenza virus, we employed mass spectrometry (MS) to search the potential binding proteins of PA subunit of H9N2. Our MS results showed that programmed cell death protein 7 (PDCD7) is a binding target of PA subunit. Co-immunoprecipitation and pull-down assays further confirmed the interaction between PDCD7 and PA subunit. Overexpression of PA subunit in A549 lung cells greatly increased the levels of PDCD7 in the nuclear and induced cell death assayed by MTT assay.Results: Flow cytometry analysis and Western blot results showed that PA subunit overexpression significantly increased the expression of pro-apoptotic protein, bax and caspase 3, and induced cell apoptosis. However, knockout of PDCD7 effectively attenuated the effects of PA overexpression in cell apoptosis.Conclusions: In conclusion, the PA subunit of H9N2 bind with PDCD7 and regulated cell apoptosis, which provide new insights in the role of PA subunit during H9N2 influenza virus infection.

scholarly journals Dual Role of Autophagy in Stress-Induced Cell Death in Rheumatoid Arthritis Synovial Fibroblasts

2013 ◽  
Vol 66 (1) ◽  
pp. 40-48 ◽  
Author(s):  
Masaru Kato ◽  
Caroline Ospelt ◽  
Renate E. Gay ◽  
Steffen Gay ◽  
Kerstin Klein
Keyword(s):  
Rheumatoid Arthritis ◽  
Cell Death ◽  
Synovial Fibroblasts ◽  
Dual Role

Role of oxidants in influenza virus-induced gene expression

1998 ◽  
Vol 274 (1) ◽  
pp. L134-L142 ◽  
Author(s):  
Katharine Knobil ◽  
Augustine M. K. Choi ◽  
Gordon W. Weigand ◽  
David B. Jacoby
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Influenza Virus ◽  
Virus Infection ◽  
A549 Cells ◽  
Influenza Virus Infection ◽  
Pyrrolidine Dithiocarbamate ◽  
Oxygen Intermediates ◽  
Mrna Induction

Influenza virus-induced epithelial damage may be mediated, in part, by reactive oxygen intermediates (ROIs). In this study, we investigated the role of ROIs in the influenza virus-induced gene expression of antioxidant enzymes and in the activation of nuclear factor-κB (NF-κB), an oxidant-sensitive transcriptional factor. Influenza virus infection increased production of intracellular ROIs in A549 pulmonary epithelial cells. Induction of manganese superoxide dismutase (MnSOD) mRNA correlated with increased MnSOD protein and enzyme activity. Influenza virus infection also activated NF-κB binding as determined by an electrophoretic mobility shift assay. Pretreatment of A549 cells with N-acetyl-l-cysteine attenuated virus-induced NF-κB activation and interleukin (IL)-8 mRNA induction but did not block induction of MnSOD mRNA. In contrast, pyrrolidine dithiocarbamate blocked activation of NF-κB and induction of MnSOD and IL-8 mRNAs. Treatment with pyrrolidine dithiocarbamate also markedly decreased virus-induced cell death. Thus oxidants are involved in influenza virus-induced activation of NF-κB, in the expression of IL-8 and MnSOD, and in virus-induced cell death.

scholarly journals Aqueous areca nut extract induces oxidative stress in human lung epithelial A549 cells: Probable role of p21 in inducing cell death

Gene Reports ◽  
2017 ◽  
Vol 6 ◽  
pp. 103-111 ◽  
Author(s):  
Rashmi Nagesh ◽  
K. M Kiran Kumar ◽  
M Naveen Kumar ◽  
Rajeshwari H. Patil ◽  
K Kavya ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Human Lung ◽  
A549 Cells ◽  
Areca Nut ◽  
Lung Epithelial ◽  
Probable Role

AB0071 Dual role of autophagy in stress-induced cell death in rheumatoid arthritis synovial fibroblasts

2013 ◽  
Vol 72 (Suppl 3) ◽  
pp. A807.2-A807
Author(s):  
M. Kato ◽  
C. Ospelt ◽  
B. A. Michel ◽  
R. E. Gay ◽  
S. Gay ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Cell Death ◽  
Synovial Fibroblasts ◽  
Dual Role

scholarly journals Dual Role of Inorganic Polyphosphate (POLYP) in the Regulation of Mitochondria-Dependent Cell Death

2017 ◽  
Vol 112 (3) ◽  
pp. 439a
Author(s):  
Maria de la Encarnacion Solesio Torregrosa ◽  
Mitchell Marta-Ariza ◽  
Fernando Goni ◽  
Evgeny V. Pavlov
Keyword(s):  
Cell Death ◽  
Dual Role ◽  
Inorganic Polyphosphate ◽  
Dependent Cell

scholarly journals Hydrogen Peroxide Causes Cell Death via Increased Transcription of HOXB13 in Human Lung Epithelial A549 Cells

Toxics ◽  
2020 ◽  
Vol 8 (4) ◽  
pp. 78
Author(s):  
Naoki Endo ◽  
Takashi Toyama ◽  
Akira Naganuma ◽  
Yoshiro Saito ◽  
Gi-Wook Hwang
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Cell Death ◽  
Human Lung ◽  
A549 Cells ◽  
Protein Levels ◽  
Intracellular Ros ◽  
Lung Epithelial ◽  
Homeobox Protein

Although homeobox protein B13 (HOXB13) is an oncogenic transcription factor, its role in stress response has rarely been examined. We previously reported that knockdown of HOXB13 reduces the cytotoxicity caused by various oxidative stress inducers. Here, we studied the role of HOXB13 in cytotoxicity caused by hydrogen peroxide in human lung epithelial A549 cells. The knockdown of HOXB13 reduced hydrogen peroxide-induced cytotoxicity; however, this phenomenon was largely absent in the presence of antioxidants (Trolox or N-acetyl cysteine (NAC)). This suggests that HOXB13 may be involved in the cytotoxicity caused by hydrogen peroxide via the production of reactive oxygen species (ROS). Hydrogen peroxide also increased both the mRNA and protein levels of HOXB13. However, these increases were rarely observed in the presence of a transcriptional inhibitor, which suggests that hydrogen peroxide increases protein levels via increased transcription of HOXB13. Furthermore, cell death occurred in A549 cells that highly expressed HOXB13. However, this cell death was mostly inhibited by treatment with antioxidants. Taken together, our findings indicate that HOXB13 may be a novel factor involved in the induction of oxidative stress, which causes cell death via intracellular ROS production.

scholarly journals Dual Role of Inflammatory Stimuli in Activation-induced Cell Death of Mouse Microglial Cells

2001 ◽  
Vol 276 (35) ◽  
pp. 32956-32965 ◽  
Author(s):  
Jongseok Lee ◽  
Jinyoung Hur ◽  
Pyeongjae Lee ◽  
Ja Young Kim ◽  
Namjoo Cho ◽  
...  
Keyword(s):  
Cell Death ◽  
Dual Role ◽  
Microglial Cells ◽  
Activation Induced Cell Death ◽  
Inflammatory Stimuli

scholarly journals Receptor-Mediated Mitophagy Rescues Cancer Cells under Hypoxic Conditions

Cancers ◽  
2021 ◽  
Vol 13 (16) ◽  
pp. 4027
Author(s):  
Alibek Abdrakhmanov ◽  
Maria A. Yapryntseva ◽  
Vitaliy O. Kaminskyy ◽  
Boris Zhivotovsky ◽  
Vladimir Gogvadze
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
A549 Cells ◽  
Inhibitory Effect ◽  
Protective Role ◽  
Hypoxic Conditions ◽  
Key Enzyme ◽  
Induced Apoptosis ◽  
Key Participants

Targeting mitochondria with thenoyltrifluoroacetone (TTFA), an inhibitor of Complex II in the respiratory chain, stimulated cisplatin-induced apoptosis in various cell lines in normoxia but not in hypoxia. This can be explained by the elimination of mitochondria involved in triggering apoptotic cell death by mitophagy, either Parkin-dependent or receptor-mediated. Treatment with TTFA alone or in combination with cisplatin did not cause accumulation of PINK1, meaning that under hypoxic conditions cells survive through activation of a receptor-mediated pathway. Hypoxia triggers the accumulation of BNIP3 and BNIP3L (also known as NIX), key participants in receptor-mediated mitophagy. Under hypoxic conditions, stimulation of autophagy, as assessed by the accumulation of lipidated form of LC3 (LC3II), was observed. To exclude the contribution of canonical macroautophagy in LC3II accumulation, experiments were performed using U1810 cells lacking ATG13, a key enzyme of macroautophagy. Despite the absence of ATG13, hypoxia-mediated accumulation of LC3II was not affected, underlying the importance of the receptor-mediated pathway. In order to prove the protective role of BNIP3 against cisplatin-induced apoptosis, BNIP3-deficient A549 cells were used. Surprisingly, a BNIP3 knockout did not abolish hypoxia-induced protection; however, in cells lacking BNIP3, a compensatory upregulation of BNIP3L was detected. Thus, in the absence of BNIP3, mitophagy could be maintained by BNIP3L and lead to cell death suppression due to the elimination of proapoptotic mitochondria. When both BNIP3 and BNIP3L were knocked out, the inhibitory effect of hypoxia on apoptosis was diminished, although not abolished completely. Undoubtedly, receptor-mediated mitophagy is likely to be one of the mechanisms responsible for cell death suppression under hypoxic conditions.

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