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Cheng Xu, Xi Chen, Wei-Bin Sheng, Peixin Yang
Autophagy is required for neurulation, and autophagy activators with minimal toxicity, such as the natural compound trehalose, a nonreducing disaccharide, possess high therapeutic value. To determine whether trehalose directly induces autophagy, FITC-labeled trehalose was used for tracing its presence in autophagosome complexes. Trehalose was as potent as rapamycin and starvation in inducing de novo autophagosome formation and increasing autophagosome flux in GFP-LC3 reporter cells and C17.2 neural stem cells...
February 12, 2019: Reproductive Toxicology
Maria Condello, Evelin Pellegrini, Michele Caraglia, Stefania Meschini
Autophagy is an evolutionarily conserved cellular process, through which damaged organelles and superfluous proteins are degraded, for maintaining the correct cellular balance during stress insult. It involves formation of double-membrane vesicles, named autophagosomes, that capture cytosolic cargo and deliver it to lysosomes, where the breakdown products are recycled back to cytoplasm. On the basis of degraded cell components, some selective types of autophagy can be identified (mitophagy, ribophagy, reticulophagy, lysophagy, pexophagy, lipophagy, and glycophagy)...
February 8, 2019: International Journal of Molecular Sciences
Ying He, Jinwoo Shin, Wanjun Gong, Pintu Das, Jinghan Qu, Zhigang Yang, Wufan Liu, Chulhun Kang, Junle Qu, Jong Seung Kim
The microviscosity change associated with reticulophagy is an important component for studying endoplasmic reticulum (ER) stress disorders. Here, a BODIPY-arsenicate conjugate 1-based fluorescent molecular rotor was designed to covalently bind vicinal dithiol-containing proteins in the ER, exhibiting a bifunction of reticulophagy initiation and microviscosity evaluation. Therefore, we could quantify the local viscosity changes during reticulophagy based on the fluorescence lifetime changes of probe 1.
February 8, 2019: Chemical Communications: Chem Comm
A Popat, A A Patel, G Warnes
The mechanistic link between ER stress, autophagy, and resultant cell death was investigated by the use of drugs Thapsigargin (Tg) and Chloroquine (CQ) with prior induction and or blockade of autophagy and apoptosis which modulated the ER stress response and resultant form of cell death. All these biological processes can be measured flow cytometrically allowing the determination of the type of cell death, G1 cell cycle arrest, cell cycle dependent measurement of ER stress transducer PERK, misfolded proteins, reticulophagy, and autophagy marker LC3B...
November 19, 2018: Cytometry. Part A: the Journal of the International Society for Analytical Cytology
Yajing Peng, Samantha L Shapiro, Varuna C Banduseela, Inca A Dieterich, Kyle J Hewitt, Emery H Bresnick, Guangyao Kong, Jing Zhang, Kathryn L Schueler, Mark P Keller, Alan D Attie, Timothy A Hacker, Ruth Sullivan, Elle Kielar-Grevstad, Sebastian I Arriola Apelo, Dudley W Lamming, Rozalyn M Anderson, Luigi Puglielli
The membrane transporter AT-1/SLC33A1 translocates cytosolic acetyl-CoA into the lumen of the endoplasmic reticulum (ER), participating in quality control mechanisms within the secretory pathway. Mutations and duplication events in AT-1/SLC33A1 are highly pleiotropic and have been linked to diseases such as spastic paraplegia, developmental delay, autism spectrum disorder, intellectual disability, propensity to seizures, and dysmorphism. Despite these known associations, the biology of this key transporter is only beginning to be uncovered...
October 2018: Aging Cell
Lawrence David Falcon Moon
After axonal injury, chromatolysis (fragmentation of Nissl substance) can occur in the soma. Electron microscopy shows that chromatolysis involves fission of the rough endoplasmic reticulum. In CNS neurons (which do not regenerate axons back to their original targets) or in motor neurons or dorsal root ganglion neurons denied axon regeneration (e.g., by transection and ligation), chromatolysis is often accompanied by degranulation (loss of ribosomes from rough endoplasmic reticulum), disaggregation of polyribosomes and degradation of monoribosomes into dust-like particles...
October 2018: Developmental Neurobiology
Matthew D Smith, Simon Wilkinson
The importance of selective macroautophagy/autophagy in cellular health is increasingly evident. The selective degradation of portions of the endoplasmic reticulum (ER), or reticulophagy, is an emerging example but requires further mechanistic detail and broad evidence of physiological relevance. In a recent study, we identified CCPG1, an ER-resident transmembrane protein that can bind to Atg8-family proteins and, independently and discretely, to RB1CC1/FIP200. Both of these interactions are required to facilitate CCPG1's function as a reticulophagy cargo receptor...
2018: Autophagy
Vikramjit Lahiri, Daniel J Klionsky
Reticulophagy is the conserved macroautophagic/autophagic degradation of the endoplasmic reticulum (ER) in response to ER stress or general nutrient deprivation. Sequestration of the ER by phagophores plays an important role in regulating ER size and homeostasis. In their recent work, Smith et al. have discovered that the ER-localized protein CCPG1 is a novel mammalian reticulophagy receptor that interacts with core autophagy machinery components-LC3, GABARAP and RB1CC1-and regulates reticulophagy.
2018: Autophagy
Hong Zhao, Mingzhu Tang, Meiqing Liu, Linxi Chen
Autophagy, a highly conserved self-digestion process, is initially regarded as non-selectively sequestering and degradation cytoplasmic contents. Nowadays, many kinds of selective autophagy have been found in response to various physiological cues such as mitophagy, reticulophagy and glycophagy. Glycophagy, as a selective autophagy, plays a crucial role in maintaining glucose homeostasis in many tissues including heart, liver and skeletal muscles. Moreover, glycophagy is highly regulated by many signal pathways like the cyclic AMP protein kinase A/protein kinase A, PI3K-Akt/PKB-mTOR and Calcium...
September 2018: Clinica Chimica Acta; International Journal of Clinical Chemistry
Julien Moretti, J Magarian Blander
Phagocytes cope with the threat of living bacteria via detection of vita-PAMPs, a specific class of pathogen-associated molecular patterns (PAMPs) that denotes microbial viability and trigger a commensurate innate response. Prokaryotic mRNA and cyclic-di-adenosine monophosphate (c-di-AMP) serve as vita-PAMPs for Gram-negative and Gram-positive bacteria, respectively, and elicit heightened proinflammatory responses not warranted for dead bacteria. The innate sensor TMEM173/STING detects c-di-AMP produced by internalized live Gram-positive bacteria, and quickly mobilizes interdependent pre-formed cell-autonomous responses including endoplasmic reticulum (ER) stress, MTOR inactivation, and reticulophagy...
2018: Autophagy
Lijun Pang, Kai Liu, Daojie Liu, Fudong Lv, Yunjin Zang, Fang Xie, Jiming Yin, Ying Shi, Yanjun Wang, Dexi Chen
Autophagy affects the pathological progression of non-alcoholic fatty liver disease (NAFLD); however, the precise role of autophagy in NAFLD remains unclear. In this study, we want to identify the role of autophagy including reticulophagy and mitophagy in NAFLD pathogenesis. When HepG2 cells were treated with 400 μM oleic acid (OA), increased reticulophagy was induced 8 h after treatment, which correlated with an anti-apoptotic response as shown by the activation of the PI3K/AKT pathway, an increase in BCL-2 expression, and the downregulation of OA-induced lipotoxicity...
January 24, 2018: Cell Death & Disease
Farhadul Islam, Vinod Gopalan, Alfred King-Yin Lam
FAM134B (family with sequence similarity 134, member B)/RETREG1 and its functional roles are relatively new in human diseases. This review aimed to summarize various functions of FAM134B since our first discovery of the gene in 2001. The protein encoded by FAM134B is a reticulophagy receptor that regulates turnover of the endoplasmic reticulum (ER) by selective phagocytosis. Absence or non-functional expression of FAM134B protein impairs ER-turnover and thereby is involved in the pathogenesis of some human diseases...
June 2018: Journal of Cellular Physiology
Liang Wang, Lei Liu, Lingsong Qin, Qingming Luo, Zhihong Zhang
Reticulophagy is a type of selective autophagy in which protein aggregate-containing and/or damaged endoplasmic reticulum (ER) fragments are engulfed for lysosomal degradation, which is important for ER homeostasis. Several chemical drugs and mutant proteins that promote protein aggregate formation within the ER lumen can efficiently induce reticulophagy in mammalian cells. However, the exact mechanism and cellular localization of reticulophagy remain unclear. In this report, we took advantage of the self-oligomerization property of p62/SQSTM1, an adaptor for selective autophagy, and developed a novel reticulophagy system based on an ER-targeted p62 mutant to investigate the process of reticulophagy in living cells...
April 2017: Science China. Life Sciences
Nicholas J Lennemann, Carolyn B Coyne
The endoplasmic reticulum (ER) is exploited by several diverse viruses during their infectious life cycles. Flaviviruses, including dengue virus (DENV) and Zika virus (ZIKV), utilize the ER as a source of membranes to establish their replication organelles and to facilitate their assembly and eventual maturation along the secretory pathway. To maintain normal homeostasis, host cells have evolved highly efficient processes to dynamically regulate the ER, such as through reticulophagy, a selective form of autophagy that leads to ER degradation...
February 2017: Autophagy
Lanfang Li, Jin Xu, Linxi Chen, Zhisheng Jiang
No abstract text is available yet for this article.
August 2016: Acta Biochimica et Biophysica Sinica
You Wang, Su-Hong Zhu, Xiu-Hua Liu
No abstract text is available yet for this article.
December 2015: Sheng Li Ke Xue Jin Zhan [Progress in Physiology]
Julia Karpeta-Kaczmarek, Maria Augustyniak, Magdalena Rost-Roszkowska
The biosafety of nanoparticles and the potential toxicity of nanopollutants and/or nanowastes are all currently burning issues. The increased use of nanoparticles, including nanodiamonds (ND), entails the real risk of their penetration into food chains, which may result in the contamination of animal and, as a result, human food. Knowledge about changes in the ultrastructure of tissues in organisms that have been exposed to ND is still very limited. The aim of the study was to describe the ultrastructure of the gut epithelium in Acheta domesticus after exposure to different concentrations of ND (0, 20 or 200 μg g(-1) - control, ND20 and ND200 groups, respectively) administered with food over a five-week period...
May 2016: Arthropod Structure & Development
Hitoshi Nakatogawa, Keisuke Mochida
Autophagy targets various intracellular components ranging from proteins and nucleic acids to organelles for their degradation in lysosomes or vacuoles. In selective types of autophagy, receptor proteins play central roles in target selection. These proteins bind or localize to specific targets, and also interact with Atg8 family proteins on forming autophagosomal membranes, leading to the efficient sequestration of the targets by the membranes. Our recent study revealed that yeast cells actively degrade the endoplasmic reticulum (ER) and even part of the nucleus via selective autophagy under nitrogen-deprived conditions...
2015: Autophagy
Andrew R Stothert, Sarah N Fontaine, Jonathan J Sabbagh, Chad A Dickey
A major drainage network involved in aqueous humor dynamics is the conventional outflow pathway, which is gated by the trabecular meshwork (TM). The TM acts as a molecular sieve, providing resistance to aqueous outflow, which is responsible for regulating intraocular pressure (IOP). If the TM is damaged, aqueous outflow is impaired, IOP increases and glaucoma can manifest. Mutations in the MYOC gene cause hereditary primary open-angle glaucoma (POAG) by promoting the abnormal amyloidosis of the myocilin protein in the endoplasmic reticulum (ER), leading to ER stress-induced TM cell death...
March 2016: Experimental Eye Research
Shane Deegan, Svetlana Saveljeva, Adrienne M Gorman, Afshin Samali
Macroautophagy (autophagy) is a cellular catabolic process which can be described as a self-cannibalism. It serves as an essential protective response during conditions of endoplasmic reticulum (ER) stress through the bulk removal and degradation of unfolded proteins and damaged organelles; in particular, mitochondria (mitophagy) and ER (reticulophagy). Autophagy is genetically regulated and the autophagic machinery facilitates removal of damaged cell components and proteins; however, if the cell stress is acute or irreversible, cell death ensues...
July 2013: Cellular and Molecular Life Sciences: CMLS
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