Concurrent induction of necrosis, apoptosis, and autophagy in ischemic preconditioned human livers formerly treated by chemotherapy

Domart, Marie-Charlotte; Esposti, Davide Degli; Sebagh, Mylène; Olaya, Natalia; Harper, Francis; Pierron, Gérard; Franc, Brigitte; Tanabe, Kenneth K.; Debuire, Brigitte; Azoulay, Daniel; Brenner, Catherine; Lemoine, Antoinette

doi:10.1016/j.jhep.2009.06.028

Cited by 51 publications

(47 citation statements)

References 35 publications

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“…Our preliminary results suggest that ER stress during PFI was reduced following IPC. Since strong correlations are observed between induction of endoplasmic reticulum (ER) stress and autophagic activation in neurodegeneration, 52,53 we propose that ER stresses in ischemic conditions are potent stimuli of autophagy in neurons.…”

Section: Methodsmentioning

confidence: 99%

Autophagy activation is associated with neuroprotection in a rat model of focal cerebral ischemic preconditioning

Sheng

Zhang²,

Rong³

et al. 2010

Autophagy

215

169

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Section: Methodsmentioning

confidence: 99%

Autophagy activation is associated with neuroprotection in a rat model of focal cerebral ischemic preconditioning

Sheng

Zhang²,

Rong³

et al. 2010

Autophagy

215

169

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show abstract

“…In addition, necrosis was reduced by IPC in the liver; however, the TUNEL assay and the expressions of caspase 3, 8, and 9 did not change. These data suggest that the activation of autophagy is involved in the IPC-induced protection against I/R through the interaction of Bcl-2 with Beclin1 and the limitation of necrosis in the human liver [70] .…”

Section: Apoptosis and Autophagymentioning

confidence: 71%

The protective roles of autophagy in ischemic preconditioning

2013

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Autophagy, a process for the degradation of protein aggregates and dysfunctional organelles, is required for cellular homeostasis and cell survival in response to stress and is implicated in endogenous protection. Ischemic preconditioning is a brief and nonlethal episode of ischemia, confers protection against subsequent ischemia-reperfusion through the up-regulation of endogenous protective mechanisms. Emerging evidence shows that autophagy is associated with the protective effect of ischemic preconditioning. This review summarizes recent progress in research on the functions and regulations of the autophagy pathway in preconditioning-induced protection and cellular survival.

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“…This is consistent with previous work performed in human livers. 24 Moreover human hepatocytes isolated from ALD livers showed no autophagy response during hypoxia and H-R possibly reflecting the extent of damage to these livers. Human hepatocytes isolated from biliary cirrhosis and normal benign liver showed similar autophagy responses in an analogous manner to the accumulation of ROS within these cells.…”

Section: Discussionmentioning

confidence: 98%

Autophagy

et al. 2012

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The role of autophagy in the response of human hepatocytes to oxidative stress remains unknown. Understanding this process may have important implications for the understanding of basic liver epithelial cell biology and the responses of hepatocytes during liver disease. To address this we isolated primary hepatocytes from human liver tissue and exposed them ex vivo to hypoxia and hypoxia-reoxygenation (H-R). We showed that oxidative stress increased hepatocyte autophagy in a reactive oxygen species (ROS) and class III PtdIns3K-dependent manner. Specifically, mitochondrial ROS and NADPH oxidase were found to be key regulators of autophagy. Autophagy involved the upregulation of BECN1, LC3A, Atg7, Atg5 and Atg 12 during hypoxia and H-R. Autophagy was seen to occur within the mitochondria of the hepatocyte and inhibition of autophagy resulted in the lowering a mitochondrial membrane potential and onset of cell death. Autophagic responses were primarily observed in the large peri-venular (PV) hepatocyte subpopulation. Inhibition of autophagy, using 3-methyladenine, increased apoptosis during H-R. Specifically, PV human hepatocytes were more susceptible to apoptosis after inhibition of autophagy. These findings show for the first time that during oxidative stress autophagy serves as a cell survival mechanism for primary human hepatocytes.

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Concurrent induction of necrosis, apoptosis, and autophagy in ischemic preconditioned human livers formerly treated by chemotherapy

Cited by 51 publications

References 35 publications

Autophagy activation is associated with neuroprotection in a rat model of focal cerebral ischemic preconditioning

Autophagy activation is associated with neuroprotection in a rat model of focal cerebral ischemic preconditioning

The protective roles of autophagy in ischemic preconditioning

Autophagy

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