scholarly journals The dual regulation of apoptosis by Flavivirus

2020 ◽  
Author(s):  
Yuhong Pan ◽  
Anchun Cheng ◽  
Mingshu Wang ◽  
Zhong Yin ◽  
Ren-Yong Jia
Keyword(s):  
Immune Response ◽  
Endoplasmic Reticulum ◽  
Signaling Pathways ◽  
Death Receptor ◽  
Scientific Basis ◽  
Research Progress ◽  
Host Defenses ◽  
Host Proteins ◽  
Infected Cells ◽  
Induced Apoptosis

Apoptosis is a form of programmed cell death, which maintains cellular homeostasis by eliminating pathogen-infected cells. It contains three signaling pathways: death receptor pathway, mitochondria-mediated pathway and endoplasmic reticulum pathway. Its importance in host defenses is highlighted by the observation that many viruses evade, hinder or destroy apoptosis, thereby weakening the host’s immune response. Flaviviruses such as Dengue virus, Japanese encephalitis virus and West Nile virus utilize various strategies to activate or inhibit cell apoptosis. This article reviews the research progress of apoptosis mechanism during flaviviruses infection, including flaviviruses proteins to regulate apoptosis by interacting with host proteins, as well as various signaling pathways involved in flaviviruses-induced apoptosis, which provides a scientific basis for understanding the pathogenesis of flaviviruses and helps in developing an effective antiviral therapy.

scholarly journals The Dual Regulation of Apoptosis by Flavivirus

2021 ◽  
Vol 12 ◽  
Author(s):  
Yuhong Pan ◽  
Anchun Cheng ◽  
Mingshu Wang ◽  
Zhongqiong Yin ◽  
Renyong Jia
Keyword(s):  
Immune Response ◽  
Endoplasmic Reticulum ◽  
Signaling Pathways ◽  
Death Receptor ◽  
Scientific Basis ◽  
Research Progress ◽  
Host Defenses ◽  
Host Proteins ◽  
Infected Cells ◽  
Induced Apoptosis

Apoptosis is a form of programmed cell death, which maintains cellular homeostasis by eliminating pathogen-infected cells. It contains three signaling pathways: death receptor pathway, mitochondria-mediated pathway, and endoplasmic reticulum pathway. Its importance in host defenses is highlighted by the observation that many viruses evade, hinder or destroy apoptosis, thereby weakening the host’s immune response. Flaviviruses such as Dengue virus, Japanese encephalitis virus, and West Nile virus utilize various strategies to activate or inhibit cell apoptosis. This article reviews the research progress of apoptosis mechanism during flaviviruses infection, including flaviviruses proteins and subgenomic flaviviral RNA to regulate apoptosis by interacting with host proteins, as well as various signaling pathways involved in flaviviruses-induced apoptosis, which provides a scientific basis for understanding the pathogenesis of flaviviruses and helps in developing an effective antiviral therapy.

scholarly journals Sulphureuine B, a drimane type sesquiterpenoid isolated from Laetiporus sulphureus induces apoptosis in glioma cells

2015 ◽  
Vol 10 (4) ◽  
pp. 844 ◽  
Author(s):  
Jing-Wei Zhang ◽  
Gong-Ling Wen ◽  
Lei Zhang ◽  
Dong-Mei Duan ◽  
Zhong-Hai Ren
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Signaling Pathways ◽  
Death Receptor ◽  
Glioma Cells ◽  
Edible Mushroom ◽  
Caspase 8 ◽  
Laetiporus Sulphureus ◽  
Death Receptor Signaling ◽  
Induced Apoptosis

<p class="Abstract">A drimane type sesquiterpenoids, sulphureuine B was isolated from the edible mushroom <em>Laetiporus sulphureus</em> and its antiproliferative properties were investigated using U-87MG glioma cells. It was observed that sulphu-reuine B-induced apoptosis in U-87MG cells and the mechanisms involved are endoplasmic reticulum stress, mitochondrial and death receptor mediated pathways. Endoplasmic reticulum stress was identified from the results of enormous cytoplasmic vacuolation, CHOP elevation and caspase-12 cleavage. Further, we found that treatment of sulphureuine B-induced PERK, IRE1α, and ATF6α activations. In addition, sulphureuine B-induced Bcl-2 down-regulation, cleavage of PARP, and caspase-8 activation were also affected. All these experimental results clearly revealed that sulphureuine B-induced apoptosis mediated through endoplasmic reticulum stress, mitochondrial, and death receptor signaling pathways.</p><p> </p>

scholarly journals Endoplasmic reticulum calcium pool depletion-induced apoptosis is coupled with activation of the death receptor 5 pathway

Oncogene ◽  
2002 ◽  
Vol 21 (17) ◽  
pp. 2623-2633 ◽  
Author(s):  
Qin He ◽  
Dong Ik Lee ◽  
Rong Rong ◽  
Myounghee Yu ◽  
Xiuquan Luo ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Death Receptor ◽  
Death Receptor 5 ◽  
Endoplasmic Reticulum Calcium ◽  
Induced Apoptosis ◽  
Calcium Pool

scholarly journals Exosomes derived from cardiac progenitor cells attenuate CVB3-induced apoptosis via abrogating the proliferation of CVB3 and modulating the mTOR signaling pathways

2019 ◽  
Vol 10 (10) ◽  
Author(s):  
Xin Li ◽  
Zuocheng Yang ◽  
Wenyuan Nie ◽  
Jie Jiang ◽  
Shentang Li ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Progenitor Cells ◽  
Viral Myocarditis ◽  
Specific Treatment ◽  
Mtor Signaling ◽  
Cardiac Progenitor Cells ◽  
H9c2 Cells ◽  
Cvb3 Infection ◽  
Infected Cells ◽  
Induced Apoptosis

Abstract Viral myocarditis is potentially fatal and lacking a specific treatment. Exosomes secreted by cardiac progenitor cells (CPCs) have emerged as a promising tool for cardioprotection and repair. In this study, we investigated whether CPCs-derived exosomes (CPCs-Ex) could utilize the mTOR signal pathway to reduce the apoptosis in viral myocarditis. In vitro, exosomes were, respectively, added to H9C2 cells after CVB3 infection to detect the anti-apoptosis effect of CPCs-Ex. Compared with the controls, the apoptosis rate was reduced, accompanied with the depressed expression of viral capsid protein 1 (VP1) and pro-apoptosis factors of Bim/caspase families. Meanwhile, the phosphorylation of Akt, mTOR, and p70S6K were promoted, but that of 4EBP1 was suppressed. In vivo, the results of apoptosis, expression of CVB3 and pro-apoptosis factors, and phosphorylation of Akt/mTOR factors of CVB3-infected cardiomyocytes were consistent with that of vitro. Following that, we use Rapamycin and MK-2206 to inhibit the Akt/mTOR signaling pathway, meanwhile, Rattus 4EBP1, p70S6K, Akt1 and Akt2 were transfected to H9C2 cells to establish the stably transfected cell lines. In the group with Rapamycin or MK-2206 pretreatment, CPCs-Ex also could decrease the apoptosis of H9C2 cells and expression of CVB3 mRNA, followed by decreased expression of apoptosis factors. In Akt2, p70S6K and 4EBP1 overexpression groups, CPCs-Ex promoted CVB3-induced apoptosis, VP1 expression and cleavage of caspase-3. Our results therefore identify CPCs-Ex exerts an anti-apoptosis effect in CVB3-infected cells by abrogating the proliferation of CVB3 and modulating the mTOR signaling pathways as well as the expression of Bcl-2 and caspase families. Viral myocarditis, mainly caused by CVB3 infection, is lacking a specific treatment. Our study identified an anti-apoptosis role of CPCs-Ex in CVB3-infected cells and rats, which shown that CPCs-Ex may be an effective tool to treat viral myocarditis. We believe that with more in-depth research on the functionality of CPCs-Ex, there will be a breakthrough in the treatment of viral myocarditis.

scholarly journals Quercetin induced apoptosis of human oral cancer SAS cells through mitochondria and endoplasmic reticulum mediated signaling pathways

2018 ◽  
Author(s):  
Yi‑Shih Ma ◽  
Chien‑Ning Yao ◽  
Hsin‑Chung Liu ◽  
Fu‑Shun Yu ◽  
Jen‑Jyh Lin ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Oral Cancer ◽  
Signaling Pathways ◽  
Induced Apoptosis

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 The Chondroprotective Role of TMF in PGE2-Induced Apoptosis Associating with Endoplasmic Reticulum Stress

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Jianqiong Yang ◽  
Haiqing Liu ◽  
Linfu Li ◽  
Hai Liu ◽  
Weimei Shi ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Signaling Pathways ◽  
Inflammatory Cytokine ◽  
Critical Role ◽  
Osteoarthritic Chondrocytes ◽  
Induced Apoptosis

Endoplasmic reticulum stress (ERS) has been demonstrated to exhibit a critical role in osteoarthritic chondrocytes. Whether 5,7,3′,4′-tetramethoxyflavone (TMF) plays the chondroprotective role in inhibition of PGE2-induced chondrocytes apoptosis associating with ERS has not been reported. To investigate this, the activation of PERK, ATF6, and IRE1 signaling pathways in ERS in chondrocytes pretreated with PGE2was studied. By treatment with PGE2, the chondrocytes apoptosis was significantly increased, the proapoptotic CHOP and JNK were upregulated, the prosurvival GRP78 and XBP1 were downregulated, and GSK-3βwas also upregulated. However, TMF exhibited the effectively protective functions via counteracting these detrimental effects of PGE2. Finally, the inflammatory cytokine PGE2can activate ERS signaling and promote chondrocytes apoptosis, which might be associated with upregulation of GSK-3β. TMF exhibits a chondroprotective role in inhibiting PGE2-induced ERS and GSK-3β.

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