Nuclear respiratory factor 1 protects H9C2 cells against hypoxia‐induced apoptosis via the death receptor pathway and mitochondrial pathway

2021 ◽  
Author(s):  
Hui Li ◽  
Nan Niu ◽  
Jihui Yang ◽  
Fei Dong ◽  
Tingrui Zhang ◽  
...  
Keyword(s):  
Death Receptor ◽  
Mitochondrial Pathway ◽  
H9c2 Cells ◽  
Death Receptor Pathway ◽  
Nuclear Respiratory Factor ◽  
Nuclear Respiratory Factor 1 ◽  
Induced Apoptosis

Hypoxia-induced apoptosis of mouse spermatocytes is mediated by HIF-1α through a death receptor pathway and a mitochondrial pathway

2017 ◽  
Vol 233 (2) ◽  
pp. 1146-1155 ◽  
Author(s):  
Jun Yin ◽  
Bing Ni ◽  
Wei-Gong Liao ◽  
Yu-Qi Gao
Keyword(s):  
Death Receptor ◽  
Mitochondrial Pathway ◽  
Death Receptor Pathway ◽  
Induced Apoptosis

scholarly journals Vesicular Stomatitis Virus Induces Apoptosis Primarily through Bak Rather than Bax by Inactivating Mcl-1 and Bcl-XL

2009 ◽  
Vol 83 (18) ◽  
pp. 9102-9112 ◽  
Author(s):  
Alicia F. Pearce ◽  
Douglas S. Lyles
Keyword(s):  
Vesicular Stomatitis Virus ◽  
Family Members ◽  
Death Receptor ◽  
Mitochondrial Pathway ◽  
Caspase 8 ◽  
Wild Type ◽  
Death Receptor Pathway ◽  
Vesicular Stomatitis ◽  
Induced Apoptosis ◽  
Interfering Rna

ABSTRACT Vesicular stomatitis virus (VSV) induces apoptosis via the mitochondrial pathway. The mitochondrial pathway is regulated by the Bcl-2 family of proteins, which consists of both pro- and antiapoptotic members. To determine the relative importance of the multidomain proapoptotic Bcl-2 family members Bak and Bax, HeLa cells were transfected with Bak and/or Bax small interfering RNA (siRNA) and subsequently infected with recombinant wild-type VSV. Our results showed that Bak is more important than Bax for the induction of apoptosis in this system. Bak is regulated by two antiapoptotic Bcl-2 proteins, Mcl-1, which is rapidly turned over, and Bcl-XL, which is relatively stable. Inhibition of host gene expression by the VSV M protein resulted in the degradation of Mcl-1 but not Bcl-XL. However, inactivation of both Mcl-1 and Bcl-XL was required for cells to undergo apoptosis. While inactivation of Mcl-1 was due to inhibition of its expression, inactivation of Bcl-XL indicates a role for one or more BH3-only Bcl-2 family members. VSV-induced apoptosis was inhibited by transfection with siRNA against Bid, a BH3-only protein that is normally activated by the cleavage of caspase-8, the initiator caspase associated with the death receptor pathway. Similarly, treatment with an inhibitor of caspase-8 inhibited VSV-induced apoptosis. These results indicate a role for cross talk from the death receptor pathway in the activation of the mitochondrial pathway by VSV.

scholarly journals Colistin-Induced Nephrotoxicity in Mice Involves the Mitochondrial, Death Receptor, and Endoplasmic Reticulum Pathways

2014 ◽  
Vol 58 (7) ◽  
pp. 4075-4085 ◽  
Author(s):  
Chongshan Dai ◽  
Jichang Li ◽  
Shusheng Tang ◽  
Jian Li ◽  
Xilong Xiao
Keyword(s):  
Endoplasmic Reticulum ◽  
Death Receptor ◽  
Mitochondrial Pathway ◽  
Protective Role ◽  
Limiting Factor ◽  
Death Domain ◽  
Tubular Necrosis ◽  
Apoptosis Pathways ◽  
Group A ◽  
Induced Apoptosis

ABSTRACTNephrotoxicity is the dose-limiting factor for colistin, but the exact mechanism is unknown. This study aimed to investigate the roles of the mitochondrial, death receptor, and endoplasmic reticulum pathways in colistin-induced nephrotoxicity. Mice were intravenously administered 7.5 or 15 mg of colistin/kg of body weight/day (via a 3-min infusion and divided into two doses) for 7 days. Renal function, oxidative stress, and apoptosis were measured. Representative biomarkers involved in the mitochondrial, death receptor, and endoplasmic reticulum pathways were investigated, and the key markers involved in apoptosis and autophagy were examined. After 7-day colistin treatment, significant increase was observed with blood urea nitrogen, serum creatinine, and malondialdehyde, while activities of superoxide dismutase (SOD) and catalase decreased in the kidneys. Acute tubular necrosis and mitochondrial dysfunction were detected, and colistin-induced apoptosis was characterized by DNA fragmentation, cleavage of poly(ADP-ribose) polymerase (PARP-1), increase of 8-hydroxydeoxyguanosine (8-OHdG), and activation of caspases (caspase-8, -9, and -3). It was evident that colistin-induced apoptosis involved the mitochondrial pathway (downregulation of Bcl-2 and upregulation of cytochrome C [cytC] and Bax), death receptor pathway (upregulation of Fas, FasL, and Fas-associated death domain [FADD]), and endoplasmic reticulum pathway (upregulation of Grp78/Bip, ATF6, GADD153/CHOP, and caspase-12). In the 15-mg/kg/day colistin group, expression of the cyclin-dependent kinase 2 (CDK2) and phosphorylated JNK (p-JNK) significantly increased (P< 0.05), while in the 7.5-mg/kg/day colistin group, a large number of autophagolysosomes and classic autophagy were observed. Western blot results of Beclin-1 and LC3B indicated that autophagy may play a protective role in colistin-induced nephrotoxicity. In conclusion, this is the first study to demonstrate that all three major apoptosis pathways and autophagy are involved in colistin-induced nephrotoxicity.

scholarly journals CLEAR AS MUD: THE TYPE I/TYPE II MODEL FOR DEATH RECEPTOR-INDUCED APOPTOSIS

2006 ◽  
Vol 43 (2) ◽  
Author(s):  
David Michael Conrad
Keyword(s):  
Death Receptor ◽  
Mitochondrial Pathway ◽  
Type I ◽  
Biological Processes ◽  
Type Ii ◽  
Type Ii Cell ◽  
Mort Cellulaire ◽  
Induced Apoptosis ◽  
First Time ◽  
The Relationship

Apoptosis is a highly organized form of cell death that plays an important regulatory role in many biological processes. The relationship between the two classical signalling pathways of apoptosis, the “death receptor” and “mitochondrial” pathways, was only vaguely appreciated until 1998, when death receptor pathway-mediated activation of the mitochondrial pathway was clearly demonstrated for the first time. The “type I/type II” model of death receptor-mediated apoptosis was proposed and subsequently adopted for use in categorizing cells according to the involvement of the mitochondrion duringdeath receptor-induced apoptosis. Since that time, however, different interpretations of the type I/type II cell definition have appeared in the literature and, consequently, the meaning of type I and type II cells has become less clear.L’apoptose est une forme de mort cellulaire très structurée qui joue un rôle important de régulation dans un grand nombre de processus biologiques. La relation entre les deux voies de signalisation traditionnelles de l’apoptose, la voie des « récepteurs de mort » et la voie mitochondriale, n’était connue que vaguement avant 1998, l'année où l’activation de la voie mitochondriale par l’intermédiaire de la voie des récepteurs de mort a été clairement démontrée pour la première fois. Le modèle « type I / type II » d’apoptose par l’intermédiaire des récepteurs de mort a été proposé puis adopté auxfins de catégorisation des cellules en fonction de la participation des mitochondries à cette apoptose. Depuis, différentes interprétations ont toutefois été formulées dans des ouvrages scientifiques quant à la définition des cellules de type I et de type II et, par conséquent, la signification de « cellules de type I » et de « cellules de type II » est devenue moins évidente.

A cytotoxic nitrido-osmium(vi) complex induces caspase-mediated apoptosis in HepG2 cancer cells

2020 ◽  
Vol 49 (47) ◽  
pp. 17173-17182
Author(s):  
Wan-Qiong Huang ◽  
Chuan-Xian Wang ◽  
Tao Liu ◽  
Zi-Xin Li ◽  
Chen Pan ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Hepg2 Cell ◽  
Cell Apoptosis ◽  
Death Receptor ◽  
Mitochondrial Pathway ◽  
Anticancer Activities ◽  
Death Receptor Pathway

A structurally fine-tuned nitridoosmium(vi) complex induces HepG2 cell apoptosis through activation of the mitochondrial pathway and death receptor pathway, showing promising in vitro and in vivo anticancer activities.

scholarly journals The Fas/Fas Ligand Death Receptor Pathway Contributes to Phenylalanine-Induced Apoptosis in Cortical Neurons

PLoS ONE ◽  
2013 ◽  
Vol 8 (8) ◽  
pp. e71553 ◽  
Author(s):  
Xiaodong Huang ◽  
Zhaohui Lu ◽  
Zhongwei Lv ◽  
Tingting Yu ◽  
Peirong Yang ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Fas Ligand ◽  
Death Receptor ◽  
Death Receptor Pathway ◽  
Induced Apoptosis

scholarly journals Celastrol-induced apoptosis in human nasopharyngeal carcinoma is associated with the activation of the death receptor and the mitochondrial pathway

2017 ◽  
Vol 14 (2) ◽  
pp. 1683-1690 ◽  
Author(s):  
Heng-Fu Lin ◽  
Ming-Ju Hsieh ◽  
Yi-Ting Hsi ◽  
Yu-Sheng Lo ◽  
Yi-Ching Chuang ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Death Receptor ◽  
Mitochondrial Pathway ◽  
Human Nasopharyngeal Carcinoma ◽  
Induced Apoptosis

scholarly journals Fas Receptor Clustering and Involvement of the Death Receptor Pathway in Rituximab-Mediated Apoptosis with Concomitant Sensitization of Lymphoma B Cells to Fas-Induced Apoptosis

2007 ◽  
Vol 178 (4) ◽  
pp. 2287-2295 ◽  
Author(s):  
Alja J. Stel ◽  
Bram ten Cate ◽  
Susan Jacobs ◽  
Jan Willem Kok ◽  
Diana C. J. Spierings ◽  
...  
Keyword(s):  
B Cells ◽  
Death Receptor ◽  
Receptor Clustering ◽  
Fas Receptor ◽  
Death Receptor Pathway ◽  
Induced Apoptosis
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