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Autophagy

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https://www.readbyqxmd.com/read/28722539/an-autophagy-driven-pathway-of-atp-secretion-supports-the-aggressive-phenotype-of-braf-v600e-inhibitor-resistant-metastatic-melanoma-cells
#1
Shaun Martin, Aleksandra M Dudek-Peric, Abhishek D Garg, Heleen Roose, Seyma Demirsoy, Sofie Van Eygen, Freya Mertens, Peter Vangheluwe, Hugo Vankelecom, Patrizia Agostinis
The ingrained capacity of melanoma cells to rapidly evolve towards an aggressive phenotype is manifested by their increased ability to develop drug-resistance, evident in the case of vemurafenib, a therapeutic-agent targeting BRAF(V600E). Previous studies indicated a tight correlation between heightened melanoma-associated macroautophagy/autophagy and acquired Vemurafenib resistance. However, how this vesicular trafficking pathway supports Vemurafenib resistance remains unclear. Here, using isogenic human and murine melanoma cell lines of Vemurafenib-resistant and patient-derived melanoma cells with primary resistance to the BRAF(V600E) inhibitor, we found that the enhanced migration and invasion of the resistant melanoma cells correlated with an enhanced autophagic capacity and autophagosome-mediated secretion of ATP...
July 19, 2017: Autophagy
https://www.readbyqxmd.com/read/28722510/bnip3l-dependent-mitophagy-accounts-for-mitochondrial-clearance-during-three-factors-induced-somatic-cell-reprogramming
#2
Ge Xiang, Liang Yang, Qi Long, Keshi Chen, Haite Tang, Yi Wu, Zihuang Liu, Yanshuang Zhou, Juntao Qi, Lingjun Zheng, Wenbo Liu, Zhongfu Ying, Weimin Fan, Hongyan Shi, Hongmei Li, Xiaobing Lin, Mi Gao, Jinglei Liu, Feixiang Bao, Linpeng Li, Lifan Duan, Min Li, Xingguo Liu
Induced pluripotent stem cells (iPSCs) have less and immature mitochondria than somatic cells and mainly rely on glycolysis for energy source. During somatic cell reprogramming, somatic mitochondria and other organelles get remodeled. However, events of organelle remodeling and interaction during somatic cell reprogramming have not been extensively explored. We show that both SKP/SKO (Sox2, Klf4, Pou5f1/Oct4) and SKPM/SKOM (SKP/SKO plus Myc/c-Myc) reprogramming lead to decreased mitochondrial mass but with different kinetics and by divergent pathways...
July 19, 2017: Autophagy
https://www.readbyqxmd.com/read/28722508/atg5-and-atg7-dependent-autophagy-in-dopaminergic-neurons-regulates-cellular-and-behavioral-responses-to-morphine
#3
Ling-Yan Su, Rongcan Luo, Qianjin Liu, Jing-Ran Su, Lu-Xiu Yang, Yu-Qiang Ding, Lin Xu, Yong-Gang Yao
The molecular basis of chronic morphine exposure remains unknown. In this study, we hypothesized that macroautophagy/autophagy of dopaminergic neurons would mediate the alterations of neuronal dendritic morphology and behavioral responses induced by morphine. Chronic morphine exposure caused Atg5 (autophagy related 5)- and Atg7 (autophagy related 7)-dependent and dopaminergic neuron-specific autophagy resulting in decreased neuron dendritic spines and the onset of addictive behaviors. In cultured primary midbrain neurons, morphine treatment significantly reduced total dendritic length and complexity, and this effect could be reversed by knockdown of Atg5 or Atg7...
July 19, 2017: Autophagy
https://www.readbyqxmd.com/read/28722507/polyglutamine-tracts-regulate-autophagy
#4
Avraham Ashkenazi, Carla F Bento, Thomas Ricketts, Mariella Vicinanza, Farah Siddiqi, Mariana Pavel, Ferdinando Squitieri, Maarten C Hardenberg, Sara Imarisio, Fiona M Menzies, David C Rubinsztein
Expansions of polyglutamine (polyQ) tracts in different proteins cause 9 neurodegenerative conditions, such as Huntington disease and various ataxias. However, many normal mammalian proteins contain shorter polyQ tracts. As these are frequently conserved in multiple species, it is likely that some of these polyQ tracts have important but unknown biological functions. Here we review our recent study showing that the polyQ domain of the deubiquitinase ATXN3/ataxin-3 enables its interaction with BECN1/beclin 1, a key macroautophagy/autophagy initiator...
July 19, 2017: Autophagy
https://www.readbyqxmd.com/read/28696138/adipoq-adiponectin-induces-cytotoxic-autophagy-in-breast-cancer-cells-through-stk11-lkb1-mediated-activation-of-the-ampk-ulk1-axis
#5
Seung J Chung, Ganji Purnachandra Nagaraju, Arumugam Nagalingam, Nethaji Muniraj, Panjamurthy Kuppusamy, Alyssa Walker, Juhyung Woo, Balázs Győrffy, Ed Gabrielson, Neeraj K Saxena, Dipali Sharma
ADIPOQ/adiponectin, an adipocytokine secreted by adipocytes in the breast tumor microenvironment, negatively regulates cancer cell growth hence increased levels of ADIPOQ/adiponectin are associated with decreased breast cancer growth. However, its mechanisms of action remain largely elusive. We report that ADIPOQ/adiponectin induces a robust accumulation of autophagosomes, increases MAP1LC3B-II/LC3B-II and decreases SQSTM1/p62 in breast cancer cells. ADIPOQ/adiponectin-treated cells and xenografts exhibit increased expression of autophagy-related proteins...
July 11, 2017: Autophagy
https://www.readbyqxmd.com/read/28633005/autophagy-impairment-mediated-by-s-nitrosation-of-atg4b-leads-to-neurotoxicity-in-response-to-hyperglycemia
#6
Yazi Li, Yuying Zhang, Lei Wang, Ping Wang, Yanhong Xue, Xiaopeng Li, Xinhua Qiao, Xu Zhang, Tao Xu, Guanghui Liu, Peng Li, Chang Chen
The majority of diabetic patients develop neuropathy and there is an increasing prevalence of neurodegeneration in the central nervous system (CNS). However, the mechanism behind is poorly understood. Here we first observed that macroautophagy/autophagy was suppressed in the hippocampus of diabetic GK rats with hyperglycemia, whereas it was unchanged in ob/ob mice without hyperglycemia. Autophagy could be directly inhibited by high glucose in mouse primary hippocampal neurons. Moreover, autophagy was protective in high-glucose-induced neurotoxicity...
June 20, 2017: Autophagy
https://www.readbyqxmd.com/read/28632995/microenvironment-and-tumors-a-nurturing-relationship
#7
Nadja Sandra Katheder, Tor Erik Rusten
No abstract text is available yet for this article.
June 20, 2017: Autophagy
https://www.readbyqxmd.com/read/28614042/bnip3l-nix-dependent-mitophagy-regulates-cell-differentiation-via-metabolic-reprogramming
#8
Lorena Esteban-Martínez, Patricia Boya
Macroautophagy/autophagy is the process by which cellular components are degraded and recycled within the lysosome. These components include mitochondria, the selective degradation of which is known as mitophagy. Mitochondria are dynamic organelles that constantly adapt their morphology, function, and number to accommodate the metabolic needs of the cell. Extensive metabolic reconfiguration occurs during cell differentiation, when mitochondrial activity increases in most cell types. However, our data demonstrate that during physiological retinal ganglion cell (RGC) development, mitophagy-dependent metabolic reprogramming towards glycolysis regulates numbers of RGCs, which are the first neurons to differentiate in the retina and whose axons form the optic nerve...
June 14, 2017: Autophagy
https://www.readbyqxmd.com/read/28614034/sqstm1-p62-sequestosome-1-senses-cellular-ubiquitin-stress-through-e2-mediated-ubiquitination
#9
Jiao Yang, Hong Peng, Xiaoduo Xie, Ronggui Hu
The alterations in cellular ubiquitin (Ub) homeostasis, known as Ub stress, feature and affect cellular responses in multiple conditions, yet the underlying mechanisms are incompletely understood. We recently report that the macroautophagy/autophagy receptor SQSTM1/p62, functions as a novel Ub sensor to activate autophagy upon Ub(+) stress (upregulation of the Ub level). First, SQSTM1 was found to undergo extensive ubiquitination and activate autophagy under Ub(+) stress induced by prolonged Bortezomib (BTZ) treatment, Ub overexpression or by heat shock...
June 14, 2017: Autophagy
https://www.readbyqxmd.com/read/28613987/methyl-%C3%AE-cyclodextrin-restores-impaired-autophagy-flux-in-niemann-pick-c1-deficient-cells-through-activation-of-ampk
#10
Sheng Dai, Andrés E Dulcey, Xin Hu, Christopher A Wassif, Forbes D Porter, Christopher P Austin, Daniel S Ory, Juan Marugan, Wei Zheng
The drug 2-hydroxypropyl-β-cyclodextrin (HPβCD) reduces lysosomal cholesterol accumulation in Niemann-Pick disease, type C (NPC) and has been advanced to human clinical trials. However, its mechanism of action for reducing cholesterol accumulation in NPC cells is uncertain and its molecular target is unknown. We found that methyl-β-cyclodextrin (MβCD), a potent analog of HPβCD, restored impaired macroautophagy/autophagy flux in Niemann-Pick disease, type C1 (NPC1) cells. This effect was mediated by a direct activation of AMP-activated protein kinase (AMPK), an upstream kinase in the autophagy pathway, through MβCD binding to its β-subunits...
June 14, 2017: Autophagy
https://www.readbyqxmd.com/read/28613983/azithromycin-attenuates-myofibroblast-differentiation-and-lung-fibrosis-development-through-proteasomal-degradation-of-nox4
#11
Kazuya Tsubouchi, Jun Araya, Shunsuke Minagawa, Hiromichi Hara, Akihiro Ichikawa, Nayuta Saito, Tsukasa Kadota, Nahoko Sato, Masahiro Yoshida, Yusuke Kurita, Kenji Kobayashi, Saburo Ito, Yu Fujita, Hirofumi Utsumi, Haruhiko Yanagisawa, Mitsuo Hashimoto, Hiroshi Wakui, Yutaka Yoshii, Takeo Ishikawa, Takanori Numata, Yumi Kaneko, Hisatoshi Asano, Makoto Yamashita, Makoto Odaka, Toshiaki Morikawa, Katsutoshi Nakayama, Yoichi Nakanishi, Kazuyoshi Kuwano
Accumulation of profibrotic myofibroblasts is involved in the process of fibrosis development during idiopathic pulmonary fibrosis (IPF) pathogenesis. TGFB (transforming growth factor β) is one of the major profibrotic cytokines for myofibroblast differentiation and NOX4 (NADPH oxidase 4) has an essential role in TGFB-mediated cell signaling. Azithromycin (AZM), a second-generation antibacterial macrolide, has a pleiotropic effect on cellular processes including proteostasis. Hence, we hypothesized that AZM may regulate NOX4 levels by modulating proteostasis machineries, resulting in inhibition of TGFB-associated lung fibrosis development...
June 14, 2017: Autophagy
https://www.readbyqxmd.com/read/28613975/activation-of-drd5-dopamine-receptor-d5-inhibits-tumor-growth-by-autophagic-cell-death
#12
Zhi Gen Leng, Shao Jian Lin, Ze Rui Wu, Yu Hang Guo, Lin Cai, Han Bing Shang, Hao Tang, Ya Jun Xue, Mei Qing Lou, Wenxiu Zhao, Wei-Dong Le, Wei Guo Zhao, Xun Zhang, Zhe Bao Wu
Dopamine agonists such as bromocriptine and cabergoline have been successfully used in the treatment of pituitary prolactinomas and other neuroendocrine tumors. However, their therapeutic mechanisms are not fully understood. In this study we demonstrated that DRD5 (dopamine receptor D5) agonists were potent inhibitors of pituitary tumor growth. We further found that DRD5 activation increased production of reactive oxygen species (ROS), inhibited the MTOR pathway, induced macroautophagy/autophagy, and led to autophagic cell death (ACD) in vitro and in vivo...
June 14, 2017: Autophagy
https://www.readbyqxmd.com/read/28613094/an-iron-hand-over-cancer-stem-cells
#13
Ahmed Hamaï, Tatiana Cañeque, Sebastian Müller, Trang Thi Mai, Antje Hienzsch, Christophe Ginestier, Emmanuelle Charafe-Jauffret, Patrice Codogno, Maryam Mehrpour, Raphaël Rodriguez
The paradigm of cancer stem cells (CSCs) defines the existence of cells exhibiting self-renewal and tumor-seeding capacity. These cells have been associated with tumor relapse and are typically resistant to conventional chemotherapeutic agents. Over the past decade, chemical biology studies have revealed a significant number of small molecules able to alter the proliferation of these cells in various settings. The natural product salinomycin has emerged as the most promising anti-CSC agent. However, an explicit mechanism of action has not yet been characterized, in particular due to the pleiotropic responses salinomycin is known for...
June 14, 2017: Autophagy
https://www.readbyqxmd.com/read/28605287/prdx1-peroxiredoxin-1-deficiency-reduces-cholesterol-efflux-via-impaired-macrophage-lipophagic-flux
#14
Se-Jin Jeong, Sinai Kim, Jong-Gil Park, In-Hyuk Jung, Mi-Ni Lee, Sejin Jeon, Hyae Yon Kweon, Dae-Yeul Yu, Sang-Hak Lee, Yangsoo Jang, Sang Won Kang, Ki-Hwan Han, Yury I Miller, Young Mi Park, Cheolho Cheong, Jae-Hoon Choi, Goo Taeg Oh
Oxidative stress activates macroautophagy/autophagy and contributes to atherogenesis via lipophagic flux, a form of lipid removal by autophagy. However, it is not known exactly how endogenous anti-oxidant enzymes are involved in lipophagic flux. Here, we demonstrate that the anti-oxidant PRDX1 (peroxiredoxin 1) has a crucial role in the maintenance of lipophagic flux in macrophages. PRDX1 is more highly expressed than other anti-oxidant enzymes in monocytes and macrophages. We determined that Prdx1 deficiency induced excessive oxidative stress and impaired maintenance of autophagic flux in macrophages...
June 12, 2017: Autophagy
https://www.readbyqxmd.com/read/28598244/accumulation-of-undegraded-autophagosomes-by-expression-of-dominant-negative-stx17-syntaxin-17-mutants
#15
Masaaki Uematsu, Taki Nishimura, Yuriko Sakamaki, Hayashi Yamamoto, Noboru Mizushima
Macroautophagy/autophagy, which is one of the main degradation systems in the cell, is mediated by a specialized organelle, the autophagosome. Purification of autophagosomes prior to fusion with lysosomes is important for both mechanistic and physiological studies of the autophagosome. Here, we report a simple method to accumulate undigested autophagosomes. Overexpression of the autophagosomal Qa-SNARE STX17 (syntaxin 17) lacking the N-terminal domain (NTD) or N-terminally tagged GFP-STX17 causes accumulation of autophagosomes...
June 9, 2017: Autophagy
https://www.readbyqxmd.com/read/28598240/classical-autophagy-proteins-lc3b-and-atg4b-facilitate-melanosome-movement-on-cytoskeletal-tracks
#16
Amrita Ramkumar, Divya Murthy, Desingu Ayyappa Raja, Archana Singh, Anusha Krishnan, Sangeeta Khanna, Archana Vats, Lipi Thukral, Pushkar Sharma, Sridhar Sivasubbu, Rajni Rani, Vivek T Natarajan, Rajesh S Gokhale
Macroautophagy/autophagy is a dynamic and inducible catabolic process that responds to a variety of hormonal and environmental cues. Recent studies highlight the interplay of this central pathway in a variety of pathophysiological diseases. Although defective autophagy is implicated in melanocyte proliferation and pigmentary disorders, the mechanistic relationship between the 2 pathways have not been elucidated. In this study, we show that autophagic proteins LC3B and ATG4B mediate melanosome trafficking on cytoskeletal tracks...
June 9, 2017: Autophagy
https://www.readbyqxmd.com/read/28598236/destructive-cellular-paths-underlying-familial-and-sporadic-parkinson-disease-converge-on-mitophagy
#17
Xinnan Wang
The knowledge gap separating the molecular and cellular underpinnings of Parkinson disease (PD) and its pathology hinders treatment innovation. Adding to this difficulty is the lack of a reliable biomarker for PD. Our previous studies identify a link of 2 PD proteins, PINK1 and PRKN/Parkin to a mitochondrial motor/adaptor RHOT1/Miro-1, which mediates mitochondrial motility and mitophagy. Here we review our recent paper showing that a third PD protein, LRRK2, also targets RHOT1 and regulates mitophagy, and pathogenic LRRK2 disrupts this function...
June 9, 2017: Autophagy
https://www.readbyqxmd.com/read/28598235/lift-and-cut-anti-host-autophagy-mechanism-of-legionella-pneumophila
#18
Supansa Pantoom, Aimin Yang, Yao-Wen Wu
RavZ, an effector protein of pathogenic Legionella pneumophila, inhibits host macroautophagy/autophagy by deconjugation of lipidated LC3 proteins from phosphatidylethanolamine (PE) on the autophagosome membrane. The mechanism for how RavZ specifically recognizes and deconjugates the lipidated LC3s is not clear. To understand the structure-function relationship of LC3-deconjugation by RavZ, we prepared semisynthetic LC3 proteins modified with different fragments of PE or 1-hexadecanol (C16). We find that RavZ activity is strictly dependent on the conjugated PE structure and RavZ extracts LC3-PE from the membrane before deconjugation...
June 9, 2017: Autophagy
https://www.readbyqxmd.com/read/28598233/functional-impairment-in-rhot1-miro1-degradation-and-mitophagy-is-a-shared-feature-in-familial-and-sporadic-parkinson-disease
#19
Vikramjit Lahiri, Daniel J Klionsky
Mitophagy is a conserved and highly regulated process of selective degradation crucial in maintaining normal cellular physiology. Genetic defects and cellular aberrations affecting mitophagy have been associated with the development of Parkinson disease. In their recently published article (highlighted in a punctum in this issue of the journal) Hsieh et al. present a putative mitophagy marker which serves as a mechanistic link between sporadic and familial Parkinson disease.
June 9, 2017: Autophagy
https://www.readbyqxmd.com/read/28598232/exercise-reestablishes-autophagic-flux-and-mitochondrial-quality-control-in-heart-failure
#20
Juliane C Campos, Bruno B Queliconi, Luiz H M Bozi, Luiz R G Bechara, Paulo M M Dourado, Allen M Andres, Paulo R Jannig, Kátia M S Gomes, Vanessa O Zambelli, Cibele Rocha-Resende, Silvia Guatimosim, Patricia C Brum, Daria Mochly-Rosen, Roberta A Gottlieb, Alicia J Kowaltowski, Julio C B Ferreira
We previously reported that facilitating the clearance of damaged mitochondria through macroautophagy/autophagy protects against acute myocardial infarction. Here we characterized the impact of exercise, a safe strategy against cardiovascular disease, on cardiac autophagy and its contribution to mitochondrial quality control, bioenergetics and oxidative damage in a post-myocardial infarction-induced heart failure animal model. We found that failing hearts displayed reduced autophagic flux depicted by accumulation of autophagy-related markers and loss of responsiveness to chloroquine treatment at 4 and 12 weeks after myocardial infarction...
June 9, 2017: Autophagy
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