We are analyzing https://link.springer.com/article/10.1007/s10495-012-0738-x.

Title:
Differential effects of the autophagy inhibitors 3-methyladenine and chloroquine on spontaneous and TNF-α-induced neutrophil apoptosis | Apoptosis
Description:
Autophagy and apoptosis cooperate to modulate cell survival. Neutrophils are short-lived cells and apoptosis is considered to be the major mechanism of their death. In the present study, we addressed whether autophagy regulates neutrophil apoptosis and investigated the effects of autophagy inhibition on apoptosis of human neutrophils. We first showed that the established autophagy inhibitors 3-methyladenine (MA) and chloroquine (CQ) markedly accelerated spontaneous neutrophil apoptosis as was evidenced by phosphatidylserine exposure, DNA fragmentation and caspase-3 activation. Apoptosis induced by the autophagy inhibitors was completely abrogated by a pan-caspase inhibitor Q-VD-OPh. Unexpectedly, both MA and CQ significantly delayed neutrophil apoptosis induced by TNF-α, although the inhibitors did attenuate late pro-survival effect of the cytokine. The effect was specific for TNF-α because it was not observed in the presence of other inflammation-associated cytokines (IL-1β or IL-8). The autophagy inhibitors did not modulate surface expression of TNF-α receptors in the absence or presence of TNF-α. Both MA and CQ induced a marked down-regulation of a key anti-apoptotic protein Mcl-1 but did not affect significantly the levels of another anti-apoptotic protein Bcl-XL. Finally, to confirm the effects of the pharmacological inhibition of autophagy by a genetic approach, we evaluated the consequences of siRNA-mediated autophagy suppression in neutrophil-like differentiated HL60 cells. Knockdown of ATG5 in the cells resulted in accelerated spontaneous apoptosis but attenuated TNF-α-induced apoptosis. Together, these data suggest that autophagy regulates neutrophil apoptosis in an inflammatory context-dependent manner and mediates the early pro-apoptotic effect of TNF-α in neutrophils.
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Keywords {🔍}

google, scholar, article, pubmed, cas, apoptosis, autophagy, neutrophil, cell, neutrophils, human, cells, death, immunol, biol, effects, mcl, mol, inhibitors, pliyev, survival, inhibition, access, spontaneous, caspase, tnfα, effect, expression, mechanisms, regulation, necrosis, privacy, cookies, content, research, differential, methyladenine, menshikov, regulates, induced, tumor, autophagic, factor, analysis, data, publish, search, chloroquine, boris, activation,

Topics {✒️}

pan-caspase inhibitor q-vd-oph tumour necrosis factor-alpha attenuated tnf-α-induced apoptosis tumor necrosis factor-alpha tnf-α-induced neutrophil apoptosis anti-apoptotic protein bcl-xl month download article/chapter inflammatory context-dependent manner sustained p38-mapk activation oncogenic ras-induced expression sirna-mediated autophagy suppression autophagosome-lysosome fusion depends early pro-apoptotic effect autophagic/lysosomal protein degradation bax-alpha-mediated regulation article apoptosis aims full article pdf nf-κb signaling related subjects pliyev & mikhail menshikov 55-kda tnf receptor programmed cell death privacy choices/manage cookies neutrophil extracellular traps asthma model induced neutrophil caspase activation cardiology research centre cell death control tnf-induced shedding constitutive neutrophil apoptosis regulating neutrophil apoptosis article pliyev modulate cell survival accelerated spontaneous apoptosis mesner pw jr tnf-α receptors selective protein kinase spontaneous apoptosis mediated human neutrophil migration cell death machinery neutrophil transendothelial migration neutrophil oxidative burst activated human neutrophils cell death mechanisms chemoattractant-activated neutrophils macroautophagy triggers apoptosis developmentally regulated manner limits clonogenic survival esquivel ja 2nd moscow state university

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