Delivery of cytoplasmic proteins to autophagosomes

Ohshiro, Kazufumi; Rayala, Suresh K.; El‐Naggar, Adel K.; Kumar, Rakesh

doi:10.4161/auto.5223

Cited by 19 publications

(18 citation statements)

References 25 publications

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“…The autophagic vacuole fraction prepared from starved rat liver was enriched with LC3-II [25]. Resveratrol has been associated with elevated autophagy and in some cases its effects have been reported to require autophagy accompanied by LC3 [22,26]. In this study, LC3-II was initially elevated in both operation groups (with/without resveratrol treatment) which might be related to the stress associated with the surgical procedures.…”

Section: Discussionmentioning

confidence: 56%

“…Autophagy plays a critical role in the management of cellular homeostasis under various stress conditions [22]. Two forms of microtubule associated protein 1 light chain 3 (LC3) are present, LC3-I is cytosolic, whereas LC3-II is membrane bound.…”

Section: Discussionmentioning

confidence: 99%

“…Autophagy can prevent cells from undergoing apoptosis by degrading damaged mitochondria [24] Autophagy is regulated by two forms of microtubule associated protein light chain 3 (LC3), LC3-I is cytosolic, whereas LC3-II is membrane bound [25]. Resveratrol has also been associated with increasing autophagy in some diseases [22,26].…”

Section: Introductionmentioning

confidence: 99%

“…Recently, autophagy has been found to be crucial in the process of cellular apoptosis induced by BDL [22]. Autophagy is active at a basal level in most of the cells in the body, and this probably reflects its role in regulating the turnover of long-lived proteins, and getting rid of damaged structures [23].…”

Section: Introductionmentioning

confidence: 99%

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The effect of the red wine polyphenol resveratrol on a rat model of biliary obstructed cholestasis: involvement of anti-apoptotic signalling, mitochondrial biogenesis and the induction of autophagy

Lin

Huang

et al. 2012

Apoptosis

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Mitochondria are known to be involved in cholestatic liver injury. The potential protective effect of resveratrol in cholestatic liver injury and the possible roles of autophagy and apoptosis induction in this process are not yet clear. The aim of this study is to determine whether resveratrol administration after bile duct ligation can reduce cholestasis-induced liver injury through modulating apoptosis, mitochondrial biogenesis and autophagy. A rat model of cholestasis was established by bile duct ligation (BDL) and compared with a sham group receiving laparotomy without BDL, with resveratrol or control treatments following BDL. The expression of proteins involved in the apoptotic and autophagic pathways were analyzed by western blotting. Apoptosis was examined by TUNEL staining. In the resveratrol/BDL group LC3-II upregulation persisted for 1-7 days, Bax was downregulated and catalase was upregulated at 3-7 days after resveratrol treatment. The decline in mitochondrial DNA copy number was reversed at 3-7 days. Caspase 3 expression was significantly downregulated at 3-7 days in the resveratrol group. TUNEL staining showed significant numbers of apoptotic liver cells appeared in livers 3-7 days after BDL and that was decreased by resveratrol treatment. Our results indicate that early resveratrol treatment reverses impaired liver function within hours of BDL.

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Section: Discussionmentioning

confidence: 56%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

The effect of the red wine polyphenol resveratrol on a rat model of biliary obstructed cholestasis: involvement of anti-apoptotic signalling, mitochondrial biogenesis and the induction of autophagy

Lin

Huang

et al. 2012

Apoptosis

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“…Autophagy prevents cells from undergoing apoptosis by degrading damaged mitochondria [11]. Resveratrol has been associated with increased autophagy in certain diseases [12,13]. …”

Section: Introductionmentioning

confidence: 99%

Resveratrol Protects Neurons and the Myocardium by Reducing Oxidative Stress and Ameliorating Mitochondria Damage in a Cerebral Ischemia Rat Model

Wang¹,

Liu²,

Liu³

et al. 2014

Cell Physiol Biochem

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Background: Resveratrol has shown potent antioxidant activity in ischemia models. The present study was performed to determine whether resveratrol protects against cerebral ischemia-induced neuronal and myocardial injury by interfering with mitochondrial homeostasis. Methods: Wistar rats were pretreated with resveratrol or vehicle intraperitoneally for one week and then subjected to cerebral ischemia via middle cerebral artery occlusion (MCAO) for 24 h. Oxidation was evaluated by quantitating SOD activity and MDA levels. Apoptosis and autophagy were measured based on TUNEL staining and the expression levels of Bcl-2, Bax and LC3II. Mitochondrial changes were evaluated by transmission electron microscopy and by analyzing the mitochondrial membrane potential. Results: Resveratrol significantly decreased mortality, neurological deficits, infarction volume and MDA levels and increased SOD activity. Furthermore, neurocyte apoptosis was alleviated by resveratrol as indicated by the increased Bcl-2/Bax ratio, increased LC3II expression and a decreased number of TUNEL-positive neurocytes. Resveratrol preserved the mitochondria in neurons and cardiomyocytes and significantly improved cardiac function. Conclusion: Resveratrol protected brain tissues against ischemic damage by interfering with mitochondrial homeostasis and inhibiting apoptosis. Furthermore, resveratrol attenuated myocardial damage, suggesting that it may be a novel therapy for cerebral ischemia diseases.

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Mammalian target of rapamycin: A valid therapeutic target through the autophagy pathway for alzheimer's disease?

Cai

Zhao

et al. 2012

J of Neuroscience Research

126

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Autophagy plays a critical role in multiple pathological lesions of Alzheimer's disease (AD), such as the formation of amyloid plaques from amyloid-β (Aβ) production and accumulation via dysregulating amyloid precursor protein turnover and enhancing the activity of β- and/or γ-secretases, intraneuronal neurofibrillary tangles (NFT) because of tau hyperphosphorylation, and neuronal apoptosis. Dysfunction of the autophagy-lysosome system also contributes to Aβ accumulation and the formation of tau oligomers and insoluble aggregates, because induction of autophagy enhances the clearance of both soluble and aggregated forms of Aβ and tau proteins. The mammalian target of rapamycin (mTOR) pathway plays a central role in controlling protein homeostasis and negatively regulates autophagy. Inhibition of mTOR by rapamycin improves cognitive deficits and rescues Aβ pathology and NFTs by increasing autophagy. Several mTOR signaling components may be potential biomarkers of cognitive impairment in the clinical diagnosis of AD. Thus, mTOR-related agents through the control of autophagy-lysosome protein degradation are emerging as an important therapeutic target for AD.

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Delivery of cytoplasmic proteins to autophagosomes

Cited by 19 publications

References 25 publications

The effect of the red wine polyphenol resveratrol on a rat model of biliary obstructed cholestasis: involvement of anti-apoptotic signalling, mitochondrial biogenesis and the induction of autophagy

The effect of the red wine polyphenol resveratrol on a rat model of biliary obstructed cholestasis: involvement of anti-apoptotic signalling, mitochondrial biogenesis and the induction of autophagy

Resveratrol Protects Neurons and the Myocardium by Reducing Oxidative Stress and Ameliorating Mitochondria Damage in a Cerebral Ischemia Rat Model

Mammalian target of rapamycin: A valid therapeutic target through the autophagy pathway for alzheimer's disease?

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