Insulin withdrawal-induced cell death in adult hippocampal neural stem cells as a model of autophagic cell death

Baek, Seung Hoon; Kim, Eun Kyoung; Goudreau, John L.; Lookingland, Keith J.; Kim, Seong Who; Yu, Sebastian

doi:10.4161/auto.5.2.7641

Cited by 35 publications

(34 citation statements)

References 14 publications

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“…So, Ras inhibition by insulin deficiencies is thought to promote neuronal apoptosis [273]. Baek et al have also reported that insulin withdrawal from HCN cells derived from adult rat brain induces autophagic cell death [274]. Elevation of cortical neuronal apoptosis in type 1 diabetic mice, reported by Li et al, is another evidence supporting the neuroprotective role of insulin [275].…”

Section: Protective Effects Against Apoptosismentioning

confidence: 94%

Insulin in the Brain: Sources, Localization and Functions

et al. 2012

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Historically, insulin is best known for its role in peripheral glucose homeostasis, and insulin signaling in the brain has received less attention. Insulin-independent brain glucose uptake has been the main reason for considering the brain as an insulin-insensitive organ. However, recent findings showing a high concentration of insulin in brain extracts, and expression of insulin receptors (IRs) in central nervous system tissues have gathered considerable attention over the sources, localization, and functions of insulin in the brain. This review summarizes the current status of knowledge of the peripheral and central sources of insulin in the brain, site-specific expression of IRs, and also neurophysiological functions of insulin including the regulation of food intake, weight control, reproduction, and cognition and memory formation. This review also considers the neuromodulatory and neurotrophic effects of insulin, resulting in proliferation, differentiation, and neurite outgrowth, introducing insulin as an attractive tool for neuroprotection against apoptosis, oxidative stress, beta amyloid toxicity, and brain ischemia.

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Section: Protective Effects Against Apoptosismentioning

confidence: 94%

Insulin in the Brain: Sources, Localization and Functions

et al. 2012

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“…118 Importantly, in recent years a causative role for autophagy in cell death could be demonstrated in certain cases through the decrease of cell death upon inactivation of an autophagy gene, often with no accompanying causative apoptotic or necrotic cell death. [119][120][121][122][123][124][125][126][127][128][129][130][131][132] The question, then, becomes not whether autophagy is causative in some cases of animal cell death (it clearly can be), but how.…”

Section: Dictyostelium Autophagic Cell Deathmentioning

confidence: 99%

Autophagy in Dictyostelium: Genes and pathways, cell death and infection

Calvo‐Garrido¹,

Carilla-Latorre²,

Kubohara³

et al. 2010

Autophagy

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“…Intriguingly, such autophagic cell death occurs in a cell with intact apoptosis machinery, but is independent of caspase activation. Therefore, it is believed that cell death in HCN stem cells induced by insulin withdrawal represents a genuine model of autophagic cell death in apoptosis-intact cells, 84,85 and fulfills the criteria we have proposed earlier in this review. Another example showing autophagy-dependent cell death under pathological conditions is hypoxia/ischemia-induced neuronal cell death in both neonatal and adult mouse brain.…”

confidence: 99%