Identification of β-chain of FoF1-ATPase in apoptotic cell population induced byMicroplitis bicoloratusbracovirus and its role in the development ofSpodoptera litura

2017 ◽  
Vol 95 (2) ◽  
pp. e21389 ◽  
Author(s):  
Tian-Chao Kou ◽  
Yue-Tong Liu ◽  
Ming Li ◽  
Yang Yang ◽  
Wei Zhang ◽  
...  
Keyword(s):  
Cell Population ◽  
Apoptotic Cell ◽  
Fof1 Atpase ◽  
Β Chain

scholarly journals Cytolethal Distending Toxin Induces Caspase-Dependent and -Independent Cell Death in MOLT-4 Cells

2008 ◽  
Vol 76 (10) ◽  
pp. 4783-4791 ◽  
Author(s):  
Masaru Ohara ◽  
Tomonori Hayashi ◽  
Yoichiro Kusunoki ◽  
Kei Nakachi ◽  
Tamaki Fujiwara ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Population ◽  
Apoptotic Cell ◽  
Flow Cytometric Analysis ◽  
Annexin V ◽  
Membrane Disruption ◽  
Classical Pathway ◽  
Cytolethal Distending Toxin ◽  
Flow Cytometric ◽  
General Caspase Inhibitor

ABSTRACT Cytolethal distending toxin (CDT) induces apoptosis using the caspase-dependent classical pathway in the majority of human leukemic T cells (MOLT-4). However, we found the process to cell death is only partially inhibited by pretreatment of the cells with a general caspase inhibitor, z-VAD-fmk. Flow cytometric analysis using annexin V and propidium iodide showed that a 48-h CDT treatment decreased the living cell population by 35% even in the presence of z-VAD-fmk. z-VAD-fmk completely inhibited caspase activity in 24 h CDT-intoxicated cells. Further, CDT with z-VAD-fmk treatment clearly increased the cell population that had a low level of intracellular reactive oxygen. This is a characteristic opposite to that of caspase-dependent apoptosis. Overexpression of bcl2 almost completely inhibited cell death using CDT treatment in the presence of z-VAD-fmk. The data suggest there are at least two different pathways used in CDT-induced cell death: conventional caspase-dependent (early) apoptotic cell death and caspase-independent (late) death. Both occur via the mitochondrial membrane disruption pathway.

scholarly journals Temporally Sensitive Trophic Responsiveness of the Adrenalectomized Rat Anterior Pituitary to Dexamethasone Challenge: Relationship between Mitotic Activity and Apoptotic Sensitivity

Endocrinology ◽  
2003 ◽  
Vol 144 (1) ◽  
pp. 212-219 ◽  
Author(s):  
L. A. Nolan ◽  
A. Levy
Keyword(s):  
Cell Cycle ◽  
Mitotic Activity ◽  
Cell Population ◽  
Anterior Pituitary ◽  
Apoptotic Cell ◽  
Apoptotic Response ◽  
Adult Rat ◽  
Step Down ◽  
Induced Apoptosis ◽  
Persistent Elevation

Abstract Depending on timing and dose, exogenous glucocorticoids induce a wave of apoptosis in the adult rat anterior pituitary, a response that is enhanced by adrenalectomy. In this study, we show that the size of the glucocorticoid-sensitive apoptotic population progressively increases during the week following surgical adrenalectomy, plateaus for a further week, then spontaneously declines to levels seen in intact animals by 4 wk. Mitotic activity, in contrast, rises rapidly post adrenalectomy but returns to baseline within 2 wk. Increased mitotic activity precedes the increase in the population of cells that undergo glucocorticoid-induced apoptosis and the subsequent decline in mitotic activity precedes the decline in apoptotic sensitivity despite persistent elevation of hypothalamic CRH and pituitary proopiomelanocortin transcripts. If glucocorticoid exposure is delayed until 4 wk post adrenalectomy when the apoptotic response has returned to baseline, glucocorticoid withdrawal, by transiently increasing mitotic activity, again primes the formation of an expanded glucocorticoid-sensitive apoptotic cell population. These data suggest that apoptotic sensitivity is largely confined to cells that have recently entered the cell cycle. This observation is further corroborated by demonstrating an abrupt glucocorticoid-induced step-down in the bromodeoxyuridine-labeling index to basal levels in rats given daily injections of bromodeoxyuridine during the week following adrenalectomy.

The expansion of a CD4+ T cell population bearing a distinctive β chain in MRLlpr/lpr mice suggests a role for the fas protein in peripheral T cell selection

1994 ◽  
Vol 24 (11) ◽  
pp. 2761-2766 ◽  
Author(s):  
Philippe Musette ◽  
Christophe Pannetier ◽  
Gabriel Gachelin ◽  
Philippe Kourilsky
Keyword(s):  
T Cell ◽  
Cell Population ◽  
Cd4 T Cell ◽  
Cell Selection ◽  
T Cell Selection ◽  
Β Chain

scholarly journals The confounding effect of interleukin-6 on apoptosis of MCF-7 cells through down-regulation of MMP-2/-9 mRNA expression

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Aybuke Celik ◽  
Filiz Bakar-Ates
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Population ◽  
Cell Morphology ◽  
Interleukin 6 ◽  
Apoptotic Cell ◽  
Dependent Manner ◽  
Rt Pcr ◽  
Down Regulation ◽  
Mcf 7

Abstract Objectives Breast cancer is the second cause of death among women worldwide. In the last decades, the immunotherapy-based approaches have a growing importance in the treatment of breast cancer. Several studies have indicated the pleiotrophic effect of Interleukin-6 (IL-6) via targeting the membrane-bound or soluble receptors. Materials and methods Different concentrations of IL-6 were incubated for 24, 48, and 72 h in the breast carcinoma cell line (MCF-7). Cell proliferation, apoptotic cell population, gene expression by RT-PCR were measured, and the effect of IL-6 treatment on cell morphology was observed. Results In the present study, IL-6 treatment of MCF-7 cells inhibited cell proliferation in a dose and time dependent manner. The IL-6 treatment was found most effective on 24 h. The viable cell amount was decreased to 70.07 ± 4.85% at 100 nM treatment with a significant alteration on cell morphology, simultaneously in the 24 h of treatment. IL-6 treatment has also increased the early apoptotic cell population % in MCF-7 cells significantly (p<0.0001). The RT-PCR analyses have shown that the apoptotic effect of IL-6 was related to the decrease at MMP-2/-9 mRNA levels (p<0.0001). Conclusions In conclusion, IL-6 treatment may inhibit cell proliferation and induce apoptosis of MCF-7 cells in a dose-dependent manner through down-regulation of MMP-2/-9.

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