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Journal articles on the topic 'Glycophagy'

To see the other types of publications on this topic, follow the link: Glycophagy.

Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Mellor, Kimberley M., Upasna Varma, David I. Stapleton, and Lea M. D. Delbridge. "Cardiomyocyte glycophagy is regulated by insulin and exposure to high extracellular glucose." American Journal of Physiology-Heart and Circulatory Physiology 306, no. 8 (April 15, 2014): H1240—H1245. http://dx.doi.org/10.1152/ajpheart.00059.2014.

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Disturbed systemic glycemic and insulinemic status elicits cardiomyocyte metabolic stress and altered glucose handling. In diabetes, pathological myocardial glycogen accumulation occurs. Recently, evidence of a specific myocardial autophagic degradation pathway for glycogen (“glycophagy”) has been reported, differentiated from the more well-characterized protein “macrophagy” pathway. The goal of this study was to identify potential mechanisms involved in cardiac glycogen accumulation, glycophagy, and macrophagy regulation using cultured neonatal rat ventricular myocytes (NRVMs). In NRVMs, insulin-induced Akt phosphorylation was evident with 5 mM-glucose conditions (∼2.3-fold increased). Under high-glucose (30 mM) conditions, insulin-augmented phosphorylation was not observed. Accumulation of glycogen was observed in response to insulin only in high-glucose conditions (∼2-fold increase). Increased expression of the glycophagy marker starch-binding domain-containing protein-1 (STBD1, 25% increase) was observed under high-glucose and insulin conditions. Expression levels of the macrophagy markers p62 and light chain protein 3BII:I were not increased by insulin at either glucose level. Preliminary results from hearts of streptozotocin-treated diabetic rats are supportive of the findings obtained in NRVMs, suggesting diabetes induced elevated expression of STBD1 and of an additional glycophagy marker GABA(A) receptor-associated protein-like 1. Confocal microscopy demonstrated that light chain protein 3B and STBD1 immunomarkers were not colocalized in NRVMs. These findings provide the first evidence that cardiomyocyte glycophagy induction occurs under the influence of insulin and is responsive to extracellular high glucose. This study suggests that the regulation of glycogen content and glycophagy induction in the cardiomyocyte may be linked, and it is speculated that glycogen pathology in diabetic cardiomyopathy has glycophagic involvement.

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2

Dong, Juan, Changquan Guo, Zhaoyu Yang, Yangyang Wu, and Caiqiao Zhang. "Follicle-Stimulating Hormone Alleviates Ovarian Aging by Modulating Mitophagy- and Glycophagy-Based Energy Metabolism in Hens." Cells 11, no. 20 (October 18, 2022): 3270. http://dx.doi.org/10.3390/cells11203270.

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As a predominant hormone in the reproductive axis, follicle-stimulating hormone (FSH) is known as the primary surviving factor for follicular growth. In this study, the alleviating effect of FSH on aging chicken granulosa cells (GCs) was investigated. Results showed that FSH activated mitophagy and relieved mitochondrial edema in D-gal-induced senescent GCs, which was evidenced by an increased number of mitophagosomes as well as increased mitochondria-light chain 3 (LC3) colocalization. Mitophagy activation was accompanied by the activation of the AMP-activated protein kinase (AMPK) signaling pathway. Furthermore, upregulated glycophagy was demonstrated by an increased interaction of starch-binding domain protein 1 (STBD1) with GABA type A receptor-associated protein-like 1 (GABARAPL1) in D-gal-induced senescent GCs. FSH treatment further promoted glycophagy, accompanied by PI3K/AKT activation. PI3K inhibitor LY294002 and AKT inhibitor GSK690693 attenuated the effect of FSH on glycophagy and glycolysis. The inhibition of FSH-mediated autophagy attenuated the protective effect of FSH on naturally aging GC proliferation and glycolysis. The simultaneous blockage of PI3K/AKT and AMPK signaling also abolished the positive effect of FSH on naturally senescent ovarian energy regulation. These data reveal that FSH prevents chicken ovarian aging by modulating glycophagy- and mitophagy-based energy metabolism through the PI3K/AKT and AMPK pathways.

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3

Zhao, Hong, Mingzhu Tang, Meiqing Liu, and Linxi Chen. "Glycophagy: An emerging target in pathology." Clinica Chimica Acta 484 (September 2018): 298–303. http://dx.doi.org/10.1016/j.cca.2018.06.014.

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4

Delbridge, Lea M. D., Kimberley M. Mellor, David J. R. Taylor, and Roberta A. Gottlieb. "Myocardial autophagic energy stress responses—macroautophagy, mitophagy, and glycophagy." American Journal of Physiology-Heart and Circulatory Physiology 308, no. 10 (May 15, 2015): H1194—H1204. http://dx.doi.org/10.1152/ajpheart.00002.2015.

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An understanding of the role of autophagic processes in the management of cardiac metabolic stress responses is advancing rapidly and progressing beyond a conceptualization of the autophagosome as a simple cell recycling depot. The importance of autophagy dysregulation in diabetic cardiomyopathy and in ischemic heart disease - both conditions comprising the majority of cardiac disease burden - has now become apparent. New findings have revealed that specific autophagic processes may operate in the cardiomyocyte, specialized for selective recognition and management of mitochondria and glycogen particles in addition to protein macromolecular structures. Thus mitophagy, glycophagy, and macroautophagy regulatory pathways have become the focus of intensive experimental effort, and delineating the signaling pathways involved in these processes offers potential for targeted therapeutic intervention. Chronically elevated macroautophagic activity in the diabetic myocardium is generally observed in association with structural and functional cardiomyopathy; yet there are also numerous reports of detrimental effect of autophagy suppression in diabetes. Autophagy induction has been identified as a key component of protective mechanisms that can be recruited to support the ischemic heart, but in this setting benefit may be mitigated by adverse downstream autophagic consequences. Recent report of glycophagy upregulation in diabetic cardiomyopathy opens up a novel area of investigation. Similarly, a role for glycogen management in ischemia protection through glycophagy initiation is an exciting prospect under investigation.

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5

Mandl, József, and Gábor Bánhegyi. "The ER – Glycogen Particle – Phagophore Triangle: A Hub Connecting Glycogenolysis and Glycophagy?" Pathology & Oncology Research 24, no. 4 (July 7, 2018): 821–26. http://dx.doi.org/10.1007/s12253-018-0446-0.

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6

Elshenawy, Dina Salem Abdelaziz, Nehal Mohammed Ramadan, Vivian Boshra Abdo, and Rehab Hamdy Ashour. "Sacubitril/valsartan combination enhanced cardiac glycophagy and prevented the progression of murine diabetic cardiomyopathy." Biomedicine & Pharmacotherapy 153 (September 2022): 113382. http://dx.doi.org/10.1016/j.biopha.2022.113382.

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7

Lajoie, Jason M., and Eric V. Shusta. "Introducing glycophage arrays: Facile production, purification and patterning of glycophages." Biotechnology Journal 10, no. 1 (October 31, 2014): 20–21. http://dx.doi.org/10.1002/biot.201400591.

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8

Reichelt, M., K. Mellor, D. Stapleton, and L. Delbridge. "Glycogen Responses During Metabolic Stress are Accentuated in Female Hearts: A Role for Myocardial Glycophagy." Heart, Lung and Circulation 22 (January 2013): S63. http://dx.doi.org/10.1016/j.hlc.2013.05.150.

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9

Reichelt, M. E., K. M. Mellor, C. L. Curl, D. Stapleton, and L. M. D. Delbridge. "Myocardial glycophagy — A specific glycogen handling response to metabolic stress is accentuated in the female heart." Journal of Molecular and Cellular Cardiology 65 (December 2013): 67–75. http://dx.doi.org/10.1016/j.yjmcc.2013.09.014.

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10

Condello, Maria, Evelin Pellegrini, Michele Caraglia, and Stefania Meschini. "Targeting Autophagy to Overcome Human Diseases." International Journal of Molecular Sciences 20, no. 3 (February 8, 2019): 725. http://dx.doi.org/10.3390/ijms20030725.

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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). Dysregulation of autophagy can induce various disease manifestations, such as inflammation, aging, metabolic diseases, neurodegenerative disorders and cancer. The understanding of the molecular mechanism that regulates the different phases of the autophagic process and the role in the development of diseases are only in an early stage. There are still questions that must be answered concerning the functions of the autophagy-related proteins. In this review, we describe the principal cellular and molecular autophagic functions, selective types of autophagy and the main in vitro methods to detect the role of autophagy in the cellular physiology. We also summarize the importance of the autophagic behavior in some diseases to provide a novel insight for target therapies.

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11

Bgatova, Nataliya P., Raushan S. Dossymbekova, Julia S. Taskaeva, Svetlana M. Miroshnichenko, Roman A. Knyazev, Anastasia O. Solovieva, Kamalidin O. Sharipov, and Zina B. Tungushbaeva. "Autophagy as a life support marker of isolated hepatocytes." Morphology 159, no. 1 (January 15, 2021): 5–12. http://dx.doi.org/10.17816/1026-3543-2021-159-1-5-12.

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AIM: The work aimed to reveal structural signs of autophagy in the cytoplasm of isolated hepatocytes in the dynamics of their cultivation. MATERIALS AND METHODS: The cultivated hepatocyte culture cell cycle was studied by flow cytofluorometry. The cells were cultured for 1, 24, and 48 hours. Morphometric analysis was performed using of the computer program Image J. The diameters of the nuclei and cytoplasm of hepatocytes, the volumes of nuclei and cytoplasm, and the nuclear-cytoplasmic ratio were determined. The concentration of intracellular organelles and autophagy was evaluated with magnification by 30000 times. RESULTS: The cell cycle arrest in the G0/G1 stage after 24 hours of hepatocyte cultivation and the preservation of their viability by hour 48 of the experiment without increase in the percentage of cells in the apoptosis stage were revealed. The decrease in the absolute count of cells was registered, as well as an increase in the nuclear-cytoplasmic ratio indicating a decrease in the proportion of hepatocyte cytoplasm in the course of cultivation. After 24 hours of cultivation, autophagosomes with fragments of cytoplasm, glycogen rosettes, and autolysosomes with partially degraded material were revealed in the cell cytoplasm. By hour 48 of the study, a significant decrease in the volume density of glycogen and mitochondria was noted, as well as an increase in basal autophagy in hepatocytes, with a prevalence of glycophagy and mitophagy. CONCLUSIONS: Autophagy maintains cellular homeostasis of isolated hepatocytes under standard culture conditions, as evidenced by a decrease in the volume density of glycogen and mitochondria, and an increase in basal autophagy in the hepatocyte cytoplasm. The findings indicate the contribution of autophagy to the survival of the primary culture of hepatocytes and can be used as an indicator of the adequacy of culturing conditions.

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12

Dürr, Clemens, Harald Nothaft, Christian Lizak, Rudi Glockshuber, and Markus Aebi. "The Escherichia coli glycophage display system." Glycobiology 20, no. 11 (June 25, 2010): 1366–72. http://dx.doi.org/10.1093/glycob/cwq102.

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13

Çelik, Eda, and Matthew P. DeLisa. "The GlycoPhage display system and its applications." New Biotechnology 29 (September 2012): S162. http://dx.doi.org/10.1016/j.nbt.2012.08.450.

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14

Counts, Brittany R., Ashok Narasimhan, Tara S. Umberger, Emma H. Doud, Amber L. Mosley, and Teresa A. Zimmers. "Abstract A062: Skeletal Muscle Selective Autophagy Receptors are induced PDAC Cachexia." Cancer Research 82, no. 22_Supplement (November 15, 2022): A062. http://dx.doi.org/10.1158/1538-7445.panca22-a062.

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Abstract Cancer-induced cachexia is a hypermetabolic condition characterized by the unintentional wasting of muscle and adipose tissue, affecting over 80% of patients with pancreatic ductal adenocarcinoma (PDAC). Muscle wasting during cachexia is due to increased skeletal muscle protein degradation via ubiquitin-proteasome and autophagy-lysosome pathways. Autophagy-lysosome degradation requires delivery of cargo to the lysosome for destruction and recycling. Macroautophagy is the most prevalent component of autophagy, encompassing bulk and selective autophagy, and it requires the de novo synthesis of an autophagosome. Bulk autophagy randomly engulfs portions of the cytoplasm. Selective autophagy is mediated through selective autophagy receptors (SAR), which bind and couple cargo to the autophagosome via the general autophagy ligands LC3B and GABARAP. While an increase in the general autophagy machinery is well described in cachectic muscle, much less is known about how complexes and organelles are selectively targeted for degradation. Methods: Here, 12-week-old male C57BL/6J mice were orthotopically implanted with 1x105 KPC cells; controls underwent sham surgery. Half of the tumor-bearing mice were treated with 120 mg/kg gemcitabine and 10 mg/kg nab-paclitaxel (GemNP) at 4 and 10 days. For endpoint analysis, mice were euthanized at 14 days when KPC mice had significant body weight, muscle mass and muscle protein loss compared to SHAM controls. In our in vitro model of PDAC cachexia, KPC-conditioned media (CM) induces C2C12 myotube wasting; thus, myotubes were treated with 50% KPC-CM or control for 48hrs. Results: GemNP reduced end tumor mass by nearly 25% and prevented body weight and muscle loss. mRNAseq of gastrocnemius muscle demonstrated induction of ribosomal component gene expression, while deep proteomics revealed reduction of 30 ribosomal component proteins in KPC mice, consistent with ongoing destruction of ribosomes. Gene expression of general autophagy ligands, LC3B (2.9-fold) and GABARAP (1.6-fold), were increased in KPC mice. Gene expression for SARs associated with ribophagy (NUFIP1, 2.6-fold) and reticulophagy (Fam134b, 11.3-fold) were increased in KPC. FAM134b protein (1.8-fold) was also increased in KPC mice. SARs for lipophagy (PNPLA2, 3.2- and PNPLA8, 1.8-fold) and mitophagy (BNIP3, 4.5-fold) were induced in KPC versus SHAM, while SARs for glycophagy and ferritinophagy were similar. SQSTM1 (3.9-fold) and NBR1 (1.9-fold), general SARs for multiple organelles including aggrephagy, lysophagy, proteaphagy and pexophagy, were increased in KPC. This activation of SARs was due to tumor-induced wasting and not chemotherapy as SAR gene expression in KPC-GemNP mice was similar to SHAM controls. Finally, we also observe markers of SAR-mediated autophagy in our in vitro model of PDAC cachexia. Conclusion: These data indicate that muscle wasting in PDAC cachexia is through activation of selective autophagy of ribosomes, mitochondria, lipid droplets, endoplasmic reticulum, protein aggregates, lysosomes, peroxisomes, and proteasomes. Citation Format: Brittany R. Counts, Ashok Narasimhan, Tara S. Umberger, Emma H. Doud, Amber L. Mosley, Teresa A. Zimmers. Skeletal Muscle Selective Autophagy Receptors are induced PDAC Cachexia [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer; 2022 Sep 13-16; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2022;82(22 Suppl):Abstract nr A062.

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15

Manj�n, A., J. Bastida, C. Romero, A. Jimeno, and J. L. Iborra. "Immobilization of naringinase on glycophase-coated porous glass." Biotechnology Letters 7, no. 7 (July 1985): 477–82. http://dx.doi.org/10.1007/bf01199862.

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16

Borrego, F., M. Tari, A. Manjon, and J. L. Iborra. "Properties of pectinesterase immobilized on glycophase-coated controlled-pore glass." Applied Biochemistry and Biotechnology 22, no. 2 (November 1989): 129–40. http://dx.doi.org/10.1007/bf02921740.

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17

Jarikote, Dilip V., Wei Li, Tao Jiang, Leif A. Eriksson, and Paul V. Murphy. "Towards echinomycin mimetics by grafting quinoxaline residues on glycophane scaffolds." Bioorganic & Medicinal Chemistry 19, no. 2 (January 2011): 826–35. http://dx.doi.org/10.1016/j.bmc.2010.12.009.

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18

Morales, Juan Carlos, and Soledad Penadés. "Kohlenhydrat-Aren-Wechselwirkungen bestimmen das Konformerengleichgewicht eines beweglichen Glycophans in Wasser." Angewandte Chemie 110, no. 5 (March 2, 1998): 673–76. http://dx.doi.org/10.1002/(sici)1521-3757(19980302)110:5<673::aid-ange673>3.0.co;2-8.

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19

Morales, Juan Carlos, and Soledad Penadés. "Carbohydrate-Arene Interactions Direct Conformational Equilibrium of a Flexible Glycophane in Water." Angewandte Chemie International Edition 37, no. 5 (March 16, 1998): 654–57. http://dx.doi.org/10.1002/(sici)1521-3773(19980316)37:5<654::aid-anie654>3.0.co;2-x.

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20

Bain, James R., and Allan S. Hoffman. "Glycophase glass revisited: protein adsorption and cell growth on glass surfaces bearing immobilized glycerol monosaccharides." Biomaterials 23, no. 16 (August 2002): 3347–57. http://dx.doi.org/10.1016/s0142-9612(02)00035-2.

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21

Leyden, Rosaria, Trinidad Velasco-Torrijos, Sabine André, Sebastien Gouin, Hans-Joachim Gabius, and Paul V. Murphy. "Synthesis of Bivalent Lactosides Based on Terephthalamide,N,N′-Diglucosylterephthalamide, and Glycophane Scaffolds and Assessment of Their Inhibitory Capacity on Medically Relevant Lectins." Journal of Organic Chemistry 74, no. 23 (December 4, 2009): 9010–26. http://dx.doi.org/10.1021/jo901667r.

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22

Manjón, A., J. L. Iborra, J. L. Gómez, E. Gómez, J. Bastida, and A. Bódalo. "Evaluation of the effectiveness factor along immobilized enzyme fixed-bed reactors: Design of a reactor with naringinase covalently immobilized into glycophase-coated porous glass." Biotechnology and Bioengineering 30, no. 4 (September 1987): 491–97. http://dx.doi.org/10.1002/bit.260300405.

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23

Napoli, Eleonora, Alexios A. Panoutsopoulos, Patricia Kysar, Nathaniel Satriya, Kira Sterling, Bradley Shibata, Denise Imai, David N. Ruskin, Konstantinos S. Zarbalis, and Cecilia Giulivi. "Wdfy3 regulates glycophagy, mitophagy, and synaptic plasticity." Journal of Cerebral Blood Flow & Metabolism, June 29, 2021, 0271678X2110273. http://dx.doi.org/10.1177/0271678x211027384.

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Autophagy is essential to cell function, as it enables the recycling of intracellular constituents during starvation and in addition functions as a quality control mechanism by eliminating spent organelles and proteins that could cause cellular damage if not properly removed. Recently, we reported on Wdfy3’s role in mitophagy, a clinically relevant macroautophagic scaffold protein that is linked to intellectual disability, neurodevelopmental delay, and autism spectrum disorder. In this study, we confirm our previous report that Wdfy3 haploinsufficiency in mice results in decreased mitophagy with accumulation of mitochondria with altered morphology, but expanding on that observation, we also note decreased mitochondrial localization at synaptic terminals and decreased synaptic density, which may contribute to altered synaptic plasticity. These changes are accompanied by defective elimination of glycogen particles and a shift to increased glycogen synthesis over glycogenolysis and glycophagy. This imbalance leads to an age-dependent higher incidence of brain glycogen deposits with cerebellar hypoplasia. Our results support and further extend Wdfy3’s role in modulating both brain bioenergetics and synaptic plasticity by including glycogen as a target of macroautophagic degradation.

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24

Koutsifeli, Parisa, Upasna Varma, Lorna J. Daniels, Marco Annandale, Xun Li, Joshua P. H. Neale, Sarah Hayes, et al. "Glycogen-autophagy: Molecular machinery and cellular mechanisms of glycophagy." Journal of Biological Chemistry, May 2022, 102093. http://dx.doi.org/10.1016/j.jbc.2022.102093.

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25

Heden, Timothy D., Lisa S. Chow, Curtis C. Hughey, and Douglas G. Mashek. "Regulation and role of glycophagy in skeletal muscle energy metabolism." Autophagy, September 10, 2021, 1–12. http://dx.doi.org/10.1080/15548627.2021.1969633.

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26

LMD, Delbridge, P. Koutsifeli, Fong SPT, M. Annandale, KL Weeks, JR Bell, and KM Mellor. "Glycophagy – the physiological perspective on a newly characterized glycogen-selective autophagy." Current Opinion in Physiology, October 2022, 100598. http://dx.doi.org/10.1016/j.cophys.2022.100598.

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27

Qiu, Fan, Yi Yuan, Wei Luo, Yan-shan Gong, Zhong-ming Zhang, Zhong-min Liu, and Ling Gao. "Asiatic acid alleviates ischemic myocardial injury in mice by modulating mitophagy- and glycophagy-based energy metabolism." Acta Pharmacologica Sinica, September 14, 2021. http://dx.doi.org/10.1038/s41401-021-00763-9.

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28

Fan, Hui, Yujia He, Junqi Xiang, Jing Zhou, Xinyan Wan, Jiawei You, Kailong Du, et al. "ROS generation attenuates the anti-cancer effect of CPX on cervical cancer cells by inducing autophagy and inhibiting glycophagy." Redox Biology, May 2022, 102339. http://dx.doi.org/10.1016/j.redox.2022.102339.

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29

Elshenawy, Dina Salem Abdelaziz, Nehal Mohammed Ramadan, Vivian Boshra Abdo, and Rehab Hamdy Ashour. "Corrigendum to “Sacubitril/valsartan combination enhanced cardiac glycophagy and prevented the progression of murine diabetic cardiomyopathy” [Biomed. Pharmacother. 153 (2022) 113382]." Biomedicine & Pharmacotherapy, October 2022, 113867. http://dx.doi.org/10.1016/j.biopha.2022.113867.

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30

& et al., Mousa. "BACILLUS MEGATERIUM BIODEGRADATION GLYCOPHATE." IRAQI JOURNAL OF AGRICULTURAL SCIENCES 50, no. 6 (December 20, 2019). http://dx.doi.org/10.36103/ijas.v50i6.859.

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This study was aimed to evaluate the Bacillus megatrium ability to growth and degradated the organophosphorus pesticides, Glyphosate. , Bacillus megaterium was isolated from Iraqi Soils and identification by morphological and biochemical tests beside a Sperber’s Medium as selectivity media. The best growth results were in (2- 60) days, had the same growth for both (5, 25) ppm on MSM. The best degradation rate ability % were in (25) ppm /60 days (70.9)%. The increasing in incubation show increasing of degradation ration% of Glyphosate via HPLC specially after 60 days , the best ration were for (25)ppm .The result is the B. megaterium used the Glyphosate as source for carbon and phosphorus and suggest could be well exploited for bioremediation of Glyphosate contaminated sites.

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31

Leyden, Rosaria, Trinidad Velasco-Torrijos, Sabine Andre, Sebastien Gouin, Hans-Joachim Gabius, and Paul V. Murphy. "ChemInform Abstract: Synthesis of Bivalent Lactosides Based on Terephthalamide, N,N′-Diglucosylterephthalamide, and Glycophane Scaffolds and Assessment of Their Inhibitory Capacity on Medically Relevant Lectins." ChemInform 41, no. 15 (April 13, 2010). http://dx.doi.org/10.1002/chin.201015192.

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