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【聚焦】走进细胞自噬 [精华]

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tangdl2000

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Autophagy. 2011 Oct 1;7(10). [Epub ahead of print]

Metabolic regulation by HMGB1-mediated autophagy and mitophagy.
代谢调节通过HMGB1介导的自噬

Kang R, Livesey KM, Zeh HJ 3rd, Loze MT, Tang D.

Source

The DAMP Laboratory; Department of Surgery; Hillman Cancer Center; University of Pittsburgh Cancer Institute; University of Pittsburgh; Pittsburgh, PA USA.

Abstract

Autophagy is a dynamic process for degradation of cytosolic components such as dysfunctional organelles and proteins and a means for generating metabolic substrates during periods of starvation. Mitochondrial autophagy ("mitophagy") is a selective form of autophagy, which is important in maintaining mitochondrial homeostasis. High mobility group box 1 (HMGB1) plays important intranuclear, cytosolic, and extracellular roles in the regulation of autophagy. Cytoplasmic HMGB1 is a novel Beclin 1-binding protein active in autophagy. Extracellular HMGB1 induces autophagy, and this role is dependent on its redox state and receptor (Receptor for Advanced Glycation End products, RAGE) expression. Nuclear HMGB1 modulates the expression of heat shock protein β-1 (HSPB1/HSP27). As a cytoskeleton regulator, HSPB1 is critical for dynamic intracellular trafficking during autophagy and mitophagy. Loss of either HMGB1 or HSPB1 results in a phenotypically similar deficiency in mitophagy typified by mitochondrial fragmentation with decreased aerobic respiration and adenosine triphosphate (ATP) production. These findings reveal a novel pathway coupling autophagy and cellular energy metabolism.

PMID: 21691146

KangAUTO7-10.pdf(869.47k)

2011-06-22 21:23

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tangdl2000

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Proc Natl Acad Sci U S A. 2011 Jun 20. [Epub ahead of print]

Ammonia-induced autophagy is independent of ULK1/ULK2 kinases.
氨诱导自噬是ULK1/2非依赖性的

Cheong H, Lindsten T, Wu J, Lu C, Thompson CB.

Source

Departments of Cancer Biology and Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104.

Abstract

Autophagy, a lysosome-mediated catabolic process, contributes to maintenance of intracellular homeostasis and cellular response to metabolic stress. In yeast, genes essential to the execution of autophagy have been defined, including autophagy-related gene 1 (ATG1), a kinase responsible for initiation of autophagy downstream of target of rapamycin. Here we investigate the role of the mammalian Atg1 homologs, uncoordinated family member (unc)-51-like kinase 1 and 2 (ULK1 and ULK2), in autophagy by generating mouse embryo fibroblasts (MEFs) doubly deficient for ULK1 and ULK2. We found that ULK1/2 are required in the autophagy response to amino acid deprivation but not for autophagy induced by deprivation of glucose or inhibition of glucose metabolism. This ULK1/2-independent autophagy was not the simple result of bioenergetic compromise and failed to be induced by AMP-activated protein kinase activators such as 5-aminoimidazole-4-carboxamide riboside and phenformin. Instead we found that autophagy induction upon glucose deprivation correlated with a rise in cellular ammonia levels caused by elevated amino acid catabolism. Even in complete medium, ammonia induced autophagy in WT and Ulk1/2(-/-) MEFs but not in Atg5-deficient MEFs. The autophagy response to ammonia is abrogated by a cell-permeable form of pyruvate resulting from the scavenging of excess ammonia through pyruvate conversion to alanine. Thus, although ULK1 and/or ULK2 are required for the autophagy response following deprivation of nitrogenous amino acids, the autophagy response to the enhanced amino acid catabolism induced by deprivation of glucose or direct exposure to ammonia does not require ULK1 and/or ULK2. Together, these data suggest that autophagy provides cells with a mechanism to adapt not only to nitrogen deprivation but also to nitrogen excess.

PMID: 21690395

1107969108.full.pdf(1451.26k)

2011-06-22 21:30

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Curr Biol. 2011 Jun 21;21(12):R478-80.

Mitochondrial dynamics: a strategy for avoiding autophagy.
线粒体动力学：避免自噬的策略

Galluzzi L, Kepp O, Kroemer G.

Source

INSERM, U848 "Apoptosis, Cancer and Immunity", F-94805 Villejuif, France; Institut Gustave Roussy, F-94805 Villejuif, France; Université Paris Sud-XI, F-94805 Villejuif, France.

Abstract

Cells normally respond to a lack of nutrients by activating autophagy, a prominent pro-survival pathway that involves the catabolism and recycling of cytoplasmic material. Recent results indicate that mitochondria actively elongate during autophagy, thereby avoiding their degradation and sustaining cell viability.

Copyright ? 2011 Elsevier Ltd. All rights reserved.

PMID: 21683905

sdarticle.pdf(1841.52k)

2011-06-22 21:34

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Mitochondrion. 2011 Jun 6. [Epub ahead of print]

Decreased heat shock protein 27 expression and altered autophagy in human cells harboring A8344G mitochondrial DNA mutation.
线粒体DNA A8344G降低热休克蛋白27的表达和自噬

Chen CY, Chen HF, Gi SJ, Chi TH, Cheng CK, Hsu CF, Ma YS, Wei YH, Liu CS, Hsieh M.

Source

Department of Life Science, TungHai University, Taichung, Taiwan, Republic of China.

Abstract

Mitochondrial DNA (mtDNA) mutations are responsible for human neuromuscular diseases caused by mitochondrial dysfunction. Myoclonus epilepsy associated with ragged-red fibers (MERRF) is a maternally inherited mitochondrial encephalomyopathy with various syndromes involving both muscular and nervous systems. The most common mutation in MERRF syndrome, A8344G mutation in mtDNA, has been associated with severe defects in protein synthesis. This defect impairs assembly of complexes in electron transport chain and results in decreased respiratory function of mitochondria. In this study, we showed a significant decrease of the heat shock protein 27 (Hsp27) in lymphoblastoid cells derived from a MERRF patient and in cybrid cells harboring MERRF A8344G mutation. However, normal cytoplasmic distributions of Hsp27 and normal heat shock responses were observed in both wild type and mutant cybrids. Furthermore, overexpression of wild type Hsp27 in mutant MERRF cybrids significantly decreased cell death under staurosporine (STS) treatment, suggesting a protective function of Hsp27 in cells harboring the A8344G mutation of mtDNA. Meanwhile, reverse transcriptase PCR showed no difference in the mRNA level between normal and mutant cybrids, indicating that alterations may occur at the protein level. Evidenced by the decreased levels of Hsp27 upon treatment with proteasome inhibitor, starvation and rapamycin and the accumulation of Hsp27 upon lysosomal inhibitor treatment; Hsp27 may be degraded by the autophagic pathway. In addition, the increased formation of LC3-II and autophagosomes was found in MERRF cybrids under the basal condition, indicating a constitutively-activated autophagic pathway. It may explain, at least partially, the faster turnover of Hsp27 in MERRF cybrids. This study provides information for us to understand that Hsp27 is degraded through the autophagic pathway and that Hsp27 may have a protective role in MERRF cells. Regulating Hsp27 and the autophagic pathway might help develop therapeutic solutions for treatment of MERRF syndrome in the future.

Copyright ? 2011 ? Elsevier B.V. and Mitochondria Research Society. All rights reserved. Published by Elsevier B.V. All rights reserved.

PMID: 21679777

2011-06-22 21:39

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