scholarly journals Autophagy Delays Apoptotic Cell Death Induced by Siniperca chuatsi Rhabdovirus in Epithelioma Papulosum Cyprinid Cells

Viruses ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1554
Author(s):  
Guang-Zhou Zhou ◽  
Jun Li ◽  
Yan-He Sun ◽  
Qin Zhang ◽  
Lu Zhang ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Fate ◽  
Apoptotic Cell ◽  
Virus Production ◽  
Host Cells ◽  
Progeny Virus ◽  
Related Factors ◽  
Apoptotic Pathway ◽  
Siniperca Chuatsi ◽  
Apoptosis Inhibitor

Autophagy and apoptosis are two key cell fate determination pathways, which play vital roles in the interaction between viruses and host cells. Previous research had confirmed that one strain of fish rhabdoviruses, Siniperca chuatsi rhabdovirus (SCRV), could induce apoptosis and autophagy after infection. In the current study, we continued to analyze the interaction of autophagy and apoptosis in SCRV-infected EPC cell lines after treatment with different autophagy or apoptosis inhibitors. We found that SCRV infection could activate the mitochondrial apoptotic pathway by the detection of the activities of the caspase-3 and caspase-9 and by flow cytometry analysis in JC-1-stained cells, respectively. Furthermore, no significant autophagy-related factors were disturbed in SCRV-infected cell after apoptosis inhibitor Z-VAD-FMK treatment, while autophagy inducer rapamycin could obviously delay the occurrence of CPE and cell death. Meanwhile, rapamycin was able to reduce the proportion of apoptotic cells. Besides that, rapamycin could disturb the expression of p62 and LC3B-II, and the transcription level of SCRV nucleoprotein mRNA. The progeny virus titers did not show a big difference between the rapamycin treatment or without it. Collectively, our data preliminarily confirmed that SCRV-activated autophagy could delay apoptosis in EPC cells and may not affect virus production. Further study may need to focus on the crosstalk regulation and its roles on the SCRV infection.

scholarly journals Increased Induction of Apoptosis by a Sendai Virus Mutant Is Associated with Attenuation of Mouse Pathogenicity

1998 ◽  
Vol 72 (4) ◽  
pp. 2927-2934 ◽  
Author(s):  
Masae Itoh ◽  
Hak Hotta ◽  
Morio Homma
Keyword(s):  
Cell Death ◽  
Dna Fragmentation ◽  
Cell Cultures ◽  
Sendai Virus ◽  
Apoptotic Cell ◽  
Virus Production ◽  
Progeny Virus ◽  
C Protein ◽  
Induction Of Apoptosis ◽  
High Degree

ABSTRACT An avirulent mutant of Sendai virus, Ohita-MVC11 (MVC11), was generated from a highly virulent field strain, Ohita-M1 (M1), through successive passages in LLC-MK2 cell cultures (M. Itoh, Y. Isegawa, H. Hotta, and M. Homma, J. Gen. Virol. 78:3207-3215, 1997). In LLC-MK2 cells, MVC11 induced a high degree of apoptotic cell death that was demonstrated by chromatin condensation of the nucleus and DNA fragmentation, and production of MVC11 declined markedly after prolonged culture. On the other hand, M1 did not induce prominent apoptosis and maintained high virus titers. In primary mouse pulmonary epithelial cell cultures, M1 replicated rather slowly to reach maximum level of virus production at 3 days postinfection, and high levels of virus production were maintained thereafter without causing apoptosis. In contrast, MVC11, which produced 20 times more progeny virus than M1 at 1 day postinfection, induced a high degree of apoptotic cell death before the virus replication cycle was completed. Accordingly, the production of progeny virus was strongly inhibited thereafter. In the lungs of mice infected with MVC11, virus antigens and signals of DNA fragmentation detected by the in situ terminal deoxynucleotidyltransferase-mediated dUTP nick end-labeling technique colocalized in bronchial epithelial cells, clearly demonstrating that infection by MVC11 triggered apoptosis in vivo as well as in vitro. These results suggest the possibility that induction of apoptosis by MVC11 plays an important role in attenuation of mouse pathogenicity by restricting progeny virus production in the lung. The C protein was shown to have the capacity to induce apoptosis, and the increased level of the C protein in MVC11-infected cells was considered to account partly, if not entirely, for the induction of apoptosis.

Activation of the intrinsic-apoptotic pathway in LNCaP prostate cancer cells by genistein- topotecan combination treatments

2013 ◽  
Vol 3 (3) ◽  
pp. 66 ◽  
Author(s):  
Vanessa Hörmann ◽  
Sivanesan Dhandayuthapani ◽  
James Kumi-Diaka ◽  
Appu Rathinavelu
Keyword(s):  
Prostate Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Apoptotic Cell ◽  
Treatment Options ◽  
Attractive Alternative ◽  
Intrinsic Apoptotic Pathway ◽  
Prostate Cancer Cells ◽  
Apoptotic Pathway ◽  
Combination Treatments

Background: Prostate cancer is the second most common cancer in American men. The development of alternative preventative and/or treatment options utilizing a combination of phytochemicals and chemotherapeutic drugs could be an attractive alternative compared to conventional carcinoma treatments. Genistein isoflavone is the primary dietary phytochemical found in soy and has demonstrated anti-tumor activities in LNCaP prostate cancer cells. Topotecan Hydrochloride (Hycamtin) is an FDA-approved chemotherapy for secondary treatment of lung, ovarian and cervical cancers. The purpose of this study was to detail the potential activation of the intrinsic apoptotic pathway in LNCaP prostate cancer cells through genistein-topotecan combination treatments. Methods: LNCaP cells were cultured in complete RPMI medium in a monolayer (70-80% confluency) at 37ºC and 5% CO2. Treatment consisted of single and combination groups of genistein and topotecan for 24 hours. The treated cells were assayed for i) growth inhibition through trypan blue exclusion assay and microphotography, ii) classification of cellular death through acridine/ ethidium bromide fluorescent staining, and iii) activation of the intrinsic apoptotic pathway through Jc-1: mitochondrial membrane potential assay, cytochrome c release and Bcl-2 protein expression.Results: The overall data indicated that genistein-topotecan combination was significantly more efficacious in reducing the prostate carcinoma’s viability compared to the single treatment options. In all treatment groups, cell death occurred primarily through the activation of the intrinsic apoptotic pathway.Conclusion: The combination of topotecan and genistein has the potential to lead to treatment options with equal therapeutic efficiency as traditional chemo- and radiation therapies, but lower cell cytotoxicity and fewer side effects in patients. Key words: topotecan; genistein; intrinsic apoptotic cell death

Presenilin-1 regulates neuronal differentiation during neurogenesis

Development ◽  
2000 ◽  
Vol 127 (12) ◽  
pp. 2593-2606 ◽  
Author(s):  
M. Handler ◽  
X. Yang ◽  
J. Shen
Keyword(s):  
Cell Death ◽  
Progenitor Cells ◽  
Neuronal Differentiation ◽  
Cell Fate ◽  
Neural Progenitor Cells ◽  
Apoptotic Cell ◽  
Ventricular Zone ◽  
Neural Progenitor ◽  
Apoptotic Cell Death ◽  
Presenilin 1

Mutations in Presenilin-1 (PS1) are a major cause of familial Alzheimer's disease. Our previous studies showed that PS1 is required for murine neural development. Here we report that lack of PS1 leads to premature differentiation of neural progenitor cells, indicating a role for PS1 in a cell fate decision between postmitotic neurons and neural progenitor cells. Neural proliferation and apoptotic cell death during neurogenesis are unaltered in PS1(−/−) mice, suggesting that the reduction in the neural progenitor cells observed in the PS1(−/−) brain is due to premature differentiation of progenitor cells, rather than to increased apoptotic cell death or decreased cell proliferation. In addition, the premature neuronal differentiation in the PS1(−/−) brain is associated with aberrant neuronal migration and disorganization of the laminar architecture of the developing cerebral hemisphere. In the ventricular zone of PS1(−/−) mice, expression of the Notch1 downstream effector gene Hes5 is reduced and expression of the Notch1 ligand Dll1 is elevated, whereas expression of Notch1 is unchanged. The level of Dll1 transcripts is also increased in the presomitic mesoderm of PS1(−/−) embryos, while the level of Notch1 transcripts is unchanged, in contrast to a previous report (Wong et al., 1997, Nature 387, 288–292). These results provide direct evidence that PS1 controls neuronal differentiation in association with the downregulation of Notch signalling during neurogenesis.

scholarly journals Genetic control of programmed cell death in the Caenorhabditis elegans hermaphrodite germline

Development ◽  
1999 ◽  
Vol 126 (5) ◽  
pp. 1011-1022 ◽  
Author(s):  
T.L. Gumienny ◽  
E. Lambie ◽  
E. Hartwieg ◽  
H.R. Horvitz ◽  
M.O. Hengartner
Keyword(s):  
Cell Death ◽  
Caenorhabditis Elegans ◽  
Germ Cell ◽  
Somatic Cell ◽  
Cell Fate ◽  
Germ Cells ◽  
Mapk Pathway ◽  
Apoptotic Cell ◽  
C Elegans ◽  
Pathway Activation

Development of the nematode Caenorhabditis elegans is highly reproducible and the fate of every somatic cell has been reported. We describe here a previously uncharacterized cell fate in C. elegans: we show that germ cells, which in hermaphrodites can differentiate into sperm and oocytes, also undergo apoptotic cell death. In adult hermaphrodites, over 300 germ cells die, using the same apoptotic execution machinery (ced-3, ced-4 and ced-9) as the previously described 131 somatic cell deaths. However, this machinery is activated by a distinct pathway, as loss of egl-1 function, which inhibits somatic cell death, does not affect germ cell apoptosis. Germ cell death requires ras/MAPK pathway activation and is used to maintain germline homeostasis. We suggest that apoptosis eliminates excess germ cells that acted as nurse cells to provide cytoplasmic components to maturing oocytes.

Filamentous actin is required for lepidopteran nucleopolyhedrovirus progeny production

Microbiology ◽  
2000 ◽  
Vol 81 (7) ◽  
pp. 1881-1888 ◽  
Author(s):  
L. M. Kasman ◽  
L. E. Volkman
Keyword(s):  
Helicoverpa Zea ◽  
Virus Production ◽  
Host Cells ◽  
Actin Binding ◽  
Anticarsia Gemmatalis ◽  
Progeny Virus ◽  
Filamentous Actin ◽  
Phylogenetic Groups ◽  
Dna Viruses ◽  
Orgyia Pseudotsugata

Autographa californica M nucleopolyhedrovirus (AcMNPV) is the prototypical member of the Nucleopolyhedrosis genus of the Baculoviridae, a family of large, double-stranded DNA viruses that are highly diverse. Nucleocapsid morphogenesis of AcMNPV and others in the Nucleopolyhedrovirus genus takes place within the nuclei of infected host cells. Previously, we showed that filamentous actin (F-actin) is essential for this process to occur in AcMNPV-infected cells, an unprecedented finding for a DNA virus that replicates within the nucleus. Because of the fundamental importance of this requirement to our understanding of virus–host interactions, and because of the diversity of viruses included within the Nucleopolyhedrovirus genus, we were compelled to determine whether the replication of other nucleopolyhedroviruses was also F-actin dependent. We report here that progeny virus production of six other lepidopteran nucleopolyhedroviruses, representing both phylogenetic groups I and II within the genus, is also F-actin dependent. The six viruses studied (Spodoptera frugiperda MNPV, Bombyx mori NPV, Orgyia pseudotsugata MNPV, Lymantria dispar MNPV, Anticarsia gemmatalis MNPV and Helicoverpa zea SNPV) were unable to produce progeny in the presence of either cytochalasin D or latrunculin A, two actin-binding agents that interfere with F-actin-dependent processes but differ in their modes of action. F-actin-dependent progeny morphogenesis, therefore, appears to be a characteristic common among viruses in this genus that have lepidopteran hosts.

scholarly journals Hsp70 Negatively Controls Rotavirus Protein Bioavailability in Caco-2 Cells Infected by the Rotavirus RF Strain

2006 ◽  
Vol 81 (3) ◽  
pp. 1297-1304 ◽  
Author(s):  
Alexis H. Broquet ◽  
Christelle Lenoir ◽  
Agnès Gardet ◽  
Catherine Sapin ◽  
Serge Chwetzoff ◽  
...  
Keyword(s):  
Viral Infection ◽  
Proteasome Inhibitors ◽  
Virus Production ◽  
Viral Proteins ◽  
Host Cells ◽  
Progeny Virus ◽  
Virus Protein ◽  
Interfering Rna ◽  
Hsp70 Induction

ABSTRACT Previous studies demonstrated that the induction of the heat shock protein Hsp70 in response to viral infection is highly specific and differs from one cell to another and for a given virus type. However, no clear consensus exists so far to explain the likely reasons for Hsp70 induction within host cells during viral infection. We show here that upon rotavirus infection of intestinal cells, Hsp70 is indeed rapidly, specifically, and transiently induced. Using small interfering RNA-Hsp70-transfected Caco-2 cells, we observed that Hsp70 silencing was associated with an increased virus protein level and enhanced progeny virus production. Upon Hsp70 silencing, we observed that the ubiquitination of the main rotavirus structural proteins was strongly reduced. In addition, the use of proteasome inhibitors in infected Caco-2 cells was shown to induce an accumulation of structural viral proteins. Together, these results are consistent with a role of Hsp70 in the control of the bioavailability of viral proteins within cells for virus morphogenesis.

The anti-apoptotic response of the Gq/11-coupled muscarinic receptor family

2003 ◽  
Vol 31 (6) ◽  
pp. 1182-1185 ◽  
Author(s):  
A.B. Tobin ◽  
D.C. Budd
Keyword(s):  
Cell Death ◽  
Muscarinic Receptor ◽  
Apoptotic Cell ◽  
Mitogen Activated Protein Kinase ◽  
Receptor Subtype ◽  
Receptor Subtypes ◽  
Muscarinic Receptor Subtypes ◽  
Structural Element ◽  
Apoptotic Pathway ◽  
Receptor Family

It is now clear that G-protein-coupled receptors can regulate programmed cell death (apoptosis) through a variety of mechanisms that are dependent on cell type and receptor subtype. Here we present evidence that the Gq/11-coupled subtypes of the muscarinic receptor family (namely M1, M3 and M5-muscarinic receptor subtypes) are able to protect against apoptotic cell death. In particular we demonstrate that the C-terminal tail of the M3-muscarinic receptor is an essential structural element for signalling to the anti-apoptotic pathway. Removal of the distal portion of the C-terminal tail results in a receptor that is coupled normally to the Gq/11/phospholipase C pathway and the mitogen-activated protein kinase pathway, but is unable to couple to the anti-apoptotic pathway. Furthermore, a poly-basic region conserved within the C-terminal tail of the Gq/11-coupled muscarinic receptor subtypes appears to be the structural determinant of coupling to the anti-apoptotic pathway.

Down-Regulation of Bax and Bak in Immuno-Chemotherapy Resistant Non-Hodgkin’s Lymphoma Cells.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 4758-4758
Author(s):  
Scott H. Olejniczak ◽  
James L. Clements ◽  
Naveen Bangia ◽  
Francisco J. Hernandez-Ilizaliturri ◽  
Myron S. Czuczman
Keyword(s):  
Cell Death ◽  
B Cell ◽  
Apoptotic Cell ◽  
Acquired Resistance ◽  
Resistant Cell ◽  
Chemotherapeutic Agents ◽  
Down Regulation ◽  
Apoptotic Pathway ◽  
B Cell Homeostasis ◽  
Limited Dilution

Abstract The balance between pro-apoptotic (Bax, Bak) and anti-apoptotic (Bcl-2, Bcl-xL, Mcl-1) Bcl-2 family proteins is essential for the maintenance of B-cell homeostasis. Disruption of this critical balance occurs in the majority of B-cell neoplasms. Clinically, high Bcl-2/Bak and Bcl-2/Bax ratios have been associated with decreased median survival (7.3 years and 3.8 years, respectively) in follicular lymphoma patients1. Recent work in mouse embryonic fibroblasts deficient for the multi-domain pro-apoptotic Bcl-2 family proteins Bax and Bak has shown that they are essential for induction of cell death following apoptotic stimuli that act through the mitochondrial (intrinsic) pathway2. The vast majority of clinically available anti-neoplastic agents, including rituximab, are known to induce cell death via this pathway and therefore likely rely on Bax and/or Bak to exert their anti-tumor effects. Alteration in expression of Bax and/or Bak could therefore underlie acquired resistance to rituximab and chemotherapy in NHL patients. To study the phenomenon of rituximab resistance we developed several rituximab-resistant cell lines (RRCL) that we subsequently showed were also resistant to chemotherapy. RRCL were generated by exposing Raji, SU-DHL-4 and RL cells to escalating doses of rituximab +/− human serum and subsequently cloning by limited dilution. In our present work we studied the efficacy of clinically-applicable chemotherapeutic agents against RRCL. Additionally we studied the intrinsic apoptotic pathway in an attempt to explain shared mechanisms of resistance to chemotherapy and rituximab. We found that RRCL have dramatically reduced levels of both Bax and Bak proteins by Western blot while levels of Bcl-2, Bcl-xL and Mcl-1 protein were comparable to parental cells. Transfection of RRCL with Bax or Bak sensitized them to apoptotic cell death. Currently, we are attempting to validate previous studies that have shown that down-regulation of Bax and/or Bak correlates with a poor prognosis in NHL. Additionally, we are exploring the mechanism(s) by which Bax and Bak are down-regulated in RRCL and primary patient samples.

scholarly journals Clarithromycin Inhibits Progeny Virus Production from Human Influenza Virus-Infected Host Cells

2008 ◽  
Vol 31 (2) ◽  
pp. 217-222 ◽  
Author(s):  
Daisei Miyamoto ◽  
Sayaka Hasegawa ◽  
Nongluk Sriwilaijaroen ◽  
Sangchai Yingsakmongkon ◽  
Hiroaki Hiramatsu ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Virus Production ◽  
Host Cells ◽  
Infected Host ◽  
Progeny Virus ◽  
Human Influenza ◽  
Human Influenza Virus ◽  
Progeny Virus Production

scholarly journals Cell adherence-promoted activity of Plesiomonas shigelloides GroEL

2007 ◽  
Vol 56 (1) ◽  
pp. 23-29 ◽  
Author(s):  
Hitoshi Tsugawa ◽  
Humie Ito ◽  
Miho Ohshima ◽  
Yoshio Okawa
Keyword(s):  
Cell Death ◽  
Nucleotide Sequence ◽  
Apoptotic Cell ◽  
Positive Influence ◽  
Host Cells ◽  
Cell Fractionation ◽  
Apoptosis Induction ◽  
Cell Adherence ◽  
Plesiomonas Shigelloides ◽  
Facscalibur Flow Cytometer

Previously, it has been demonstrated that the invasion of Caco-2 cells by Plesiomonas shigelloides induces apoptotic cell death. Therefore, the attachment to and colonization of eukaryotic intestinal host cells by P. shigelloides are important steps in causing pathogenicity. In this study, the participation of P. shigelloides GroEL in the attachment of P. shigelloides was examined. The groESL operon of P. shigelloides was isolated by PCR. The nucleotide sequence of the groESL operon of P. shigelloides revealed two ORFs of 294 nucleotides for groES and 1647 nucleotides for groEL. Cell fractionation and immunostaining experiments suggested that the GroEL of P. shigelloides was associated with the bacterial cell surface. The expression of the groEL gene was upregulated during the attachment and apoptosis-induction stages, and the expression of the protein was also induced during the attachment stage. Furthermore, GroEL efficiently promoted the attachment of P. shigelloides to Caco-2 cells, as measured by a FACSCalibur flow cytometer. These results demonstrated that GroEL has a positive influence on the attachment of P. shigelloides to Caco-2 cells.

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