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https://www.readbyqxmd.com/read/28738171/emerging-roles-for-tfeb-in-the-immune-response-and-inflammation
#1
Owen A Brady, José A Martina, Rosa Puertollano
Inflammation is a central feature of an effective immune response, which functions to eliminate pathogens and other foreign material, and promote recovery; however, dysregulation of the inflammatory response is associated with a wide variety of disease states. The autophagy-lysosome pathway is one of 2 major degradative pathways used by the cell and serves to eliminate long-lived and dysfunctional proteins and organelles to maintain homeostasis. Mounting evidence implicates the autophagy-lysosome pathway as a key player in regulating the inflammatory response; hence many inflammatory diseases may fundamentally be diseases of autophagy-lysosome pathway dysfunction...
July 24, 2017: Autophagy
https://www.readbyqxmd.com/read/28724634/adaptor-protein-p62-promotes-skin-tumor-growth-and-metastasis-and-is-induced-by-uva-radiation
#2
Ashley Sample, Baozhong Zhao, Lei Qiang, Yu-Ying He
Skin cancer is the most common cancer and exposure to ultraviolet (UV) radiation, namely UVA and UVB is the major risk factor for skin cancer development. UVA is significantly less effective in causing direct DNA damage than UVB, but UVA has been shown to increase skin cancer risk. The mechanism by which UVA contributes to skin cancer remains unclear. Here, using RNA-Seq, we show that UVA induces autophagy and lysosomal gene expression, including the autophagy receptor and substrate p62. We found that UVA activates the transcription factor EB (TFEB), a known regulator of autophagy and lysosomal gene expression, which, in turn, induces p62 transcription...
July 19, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28720712/regulation-of-the-autophagy-system-during-chronic-contractile-activity-induced-muscle-adaptations
#3
Yuho Kim, David A Hood
Skeletal muscle is adaptable to exercise stimuli via the upregulation of mitochondrial biogenesis, and recent studies have suggested that autophagy also plays a role in exercise-induced muscle adaptations. However, it is still obscure how muscle regulates autophagy over the time course of training adaptations. This study examined the expression of autophagic proteins in skeletal muscle of rats exposed to chronic contractile activity (CCA; 6 h/day, 9V, 10 Hz continuous, 0.1 msec pulse duration) for 1, 3, and 7 days (n = 8/group)...
July 2017: Physiological Reports
https://www.readbyqxmd.com/read/28712747/selectivity-and-kinetic-requirements-of-hdac-inhibitors-as-progranulin-enhancers-for-treating-frontotemporal-dementia
#4
Angela She, Iren Kurtser, Surya A Reis, Krista Hennig, Jenny Lai, Audrey Lang, Wen-Ning Zhao, Ralph Mazitschek, Bradford C Dickerson, Joachim Herz, Stephen J Haggarty
Frontotemporal dementia (FTD) arises from neurodegeneration in the frontal, insular, and anterior temporal lobes. Autosomal dominant causes of FTD include heterozygous mutations in the GRN gene causing haploinsufficiency of progranulin (PGRN) protein. Recently, histone deacetylase (HDAC) inhibitors have been identified as enhancers of PGRN expression, although the mechanisms through which GRN is epigenetically regulated remain poorly understood. Using a chemogenomic toolkit, including optoepigenetic probes, we show that inhibition of class I HDACs is sufficient to upregulate PGRN in human neurons, and only inhibitors with apparent fast binding to their target HDAC complexes are capable of enhancing PGRN expression...
July 20, 2017: Cell Chemical Biology
https://www.readbyqxmd.com/read/28700687/secretory-carrier-membrane-protein-5-is-an-autophagy-inhibitor-that-promotes-the-secretion-of-%C3%AE-synuclein-via-exosome
#5
Yi Yang, Meiling Qin, Puhua Bao, Wangchao Xu, Jin Xu
Autophagy-lysosomal pathway is a cellular protective system to remove aggregated proteins and damaged organelles. Meanwhile, exosome secretion has emerged as a mode to selectively clear the neurotoxic proteins, such as α-synuclein. Mounting evidence suggests that these two cellular processes are coordinated to facilitate the clearance of toxic cellular waste; however the regulators for the transition between these two processes are unclear. Here we show that SCAMP5, a secretory carrier membrane protein significantly induced in the brains of Huntington's disease patients, is quickly and transiently induced by protein stress and autophagic stimulation, and is regulated by the master autophagy transcriptional regulator TFEB...
2017: PloS One
https://www.readbyqxmd.com/read/28697598/nox2-mediated-tfeb-activation-and-vacuolization-regulate-lysosome-associated-cell-death-induced-by-gypenoside-l-a-saponin-isolated-from-gynostemma-pentaphyllum
#6
Kai Zheng, Yingchun Jiang, Chenghui Liao, Xiaopeng Hu, Yan Li, Yong Zeng, Jian Zhang, Xuli Wu, Haiqiang Wu, Lizhong Liu, Yifei Wang, Zhendan He
Tumor cells frequently obtain their chemoresistance through deregulating apoptotic signaling and activating protective autophagy. Therefore, exploring efficient chemotherapeutic agents or isolating novel natural products that can trigger non-apoptotic and non-autophagic cell death such as lysosome-associated death is emergently required. We have recently shown that Gypenoside L (Gyp-L), a saponin isolated from Gynostemma pentaphyllum, induces lysosome swelling and cell death in esophageal cancer cells. However, contributions of vacuolization and lysosome to cell death remain unclear...
July 11, 2017: Journal of Agricultural and Food Chemistry
https://www.readbyqxmd.com/read/28688268/tfeb-mediated-activation-of-the-lysosome-autophagy-system-affects-the-transduction-efficiency-of-adeno-associated-virus-2
#7
Lauren Popp, Eric Gomez, Whitney Orji, Michelle Ho, Junghae Suh, Laura Segatori
Adeno-associated virus (AAV)-mediated gene transfer is an appealing therapeutic option due to AAV's safety profile. Effective delivery of AAV's genetic cargo to the nucleus, however, requires evasion of host cell barriers, including cellular clearance mechanisms mediated by the lysosome-autophagy system. We used AAV serotype 2 to monitor the autophagic response to cellular internalization of AAV and to characterize the effect of AAV-induced activation of autophagy on transgene expression. We found AAV2 internalization to induce activation of transcription factor EB, a master regulator of autophagy and lysosomal biogenesis, and upregulation of the lysosome-autophagy system...
July 5, 2017: Virology
https://www.readbyqxmd.com/read/28656016/the-transcription-factor-eb-links-cellular-stress-to-the-immune-response%C3%A2-%C3%A2
#8
REVIEW
Neel R Nabar, John H Kehrl
The transcription factor EB (TFEB) is the master transcriptional regulator of autophagy and lysosome biogenesis. Recent advances have led to a paradigm shift in our understanding of lysosomes from a housekeeping cellular waste bin to a dynamically regulated pathway that is efficiently turned up or down based on cellular needs. TFEB coordinates the cellular response to nutrient deprivation and other forms of cell stress through the lysosome system, and regulates a myriad of cellular processes associated with this system including endocytosis, phagocytosis, autophagy, and lysosomal exocytosis...
June 2017: Yale Journal of Biology and Medicine
https://www.readbyqxmd.com/read/28638736/transcriptional-factor-eb-regulates-macrophage-polarization-in-the-tumor-microenvironment
#9
Liang Fang, Johnie Hodge, Fatma Saaoud, Junfeng Wang, Stephen Iwanowycz, Yuzhen Wang, Yvonne Hui, Trent D Evans, Babak Razani, Daping Fan
Tumor microenvironment (TME) contains a variety of infiltrating immune cells. Among them, tumor-associated macrophages (TAMs) and their alternative activation contribute greatly to the progression of tumors. The mechanisms governing macrophage polarization in the TME are unclear. Here, we show that in TAMs or macrophages under tumor-conditioned medium treatment, the expression of transcription factor EB (TFEB) is reduced and more of the TFEB protein is in an inactive cytosolic form. Transforming growth factor (TGF)-β is identified as a main driving force for the reduced TFEB expression and activity in TAMs via activating ERK signaling...
2017: Oncoimmunology
https://www.readbyqxmd.com/read/28637240/tfeb-activation-restores-migration-ability-to-tsc1-deficient-adult-neural-stem-progenitor-cells
#10
Alessandro Magini, Alice Polchi, Danila Di Meo, Giuseppina Mariucci, Krizia Sagini, Federico De Marco, Tommaso Cassano, Stefano Giovagnoli, Diego Dolcetta, Carla Emiliani
Tuberous sclerosis complex (TSC) is an autosomal dominant genetic disorder caused by mutations in either of two genes, TSC1 or TSC2, resulting in the constitutive activation of the mammalian target of rapamycin complex 1 (mTORC1). mTOR inhibitors are now considered the treatment of choice for TSC disease. A major pathological feature of TSC is the development of subependymal giant cell astrocytomas (SEGAs) in the brain. Nowadays, it is thought that SEGAs could be a consequence of aberrant aggregation and migration of neural stem/progenitor cells (NSPCs)...
June 14, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28636416/akt-modulates-the-autophagy-lysosome-pathway-via-tfeb
#11
Michela Palmieri, Rituraj Pal, Marco Sardiello
No abstract text is available yet for this article.
June 21, 2017: Cell Cycle
https://www.readbyqxmd.com/read/28629821/glycogen-reduction-in-myotubes-of-late-onset-pompe-disease-patients-using-antisense-technology
#12
Elisa Goina, Paolo Peruzzo, Bruno Bembi, Andrea Dardis, Emanuele Buratti
Glycogen storage disease type II (GSDII) is a lysosomal disorder caused by the deficient activity of acid alpha-glucosidase (GAA) enzyme, leading to the accumulation of glycogen within the lysosomes. The disease has been classified in infantile and late-onset forms. Most late-onset patients share a splicing mutation c.-32-13T > G in intron 1 of the GAA gene that prevents efficient recognition of exon 2 by the spliceosome. In this study, we have mapped the splicing silencers of GAA exon 2 and developed antisense morpholino oligonucleotides (AMOs) to inhibit those regions and rescue normal splicing in the presence of the c...
June 16, 2017: Molecular Therapy: the Journal of the American Society of Gene Therapy
https://www.readbyqxmd.com/read/28607479/corrigendum-mtorc1-independent-tfeb-activation-via-akt-inhibition-promotes-cellular-clearance-in-neurodegenerative-storage-diseases
#13
Michela Palmieri, Rituraj Pal, Hemanth R Nelvagal, Parisa Lotfi, Gary R Stinnett, Michelle L Seymour, Arindam Chaudhury, Lakshya Bajaj, Vitaliy V Bondar, Laura Bremner, Usama Saleem, Dennis Y Tse, Deepthi Sanagasetti, Samuel M Wu, Joel R Neilson, Fred A Pereira, Robia G Pautler, George G Rodney, Jonathan D Cooper, Marco Sardiello
This corrects the article DOI: 10.1038/ncomms14338.
June 13, 2017: Nature Communications
https://www.readbyqxmd.com/read/28589926/exploiting-macrophage-autophagy-lysosomal-biogenesis-as-a-therapy-for-atherosclerosis
#14
Ismail Sergin, Trent D Evans, Xiangyu Zhang, Somashubhra Bhattacharya, Carl J Stokes, Eric Song, Sahl Ali, Babak Dehestani, Karyn B Holloway, Paul S Micevych, Ali Javaheri, Jan R Crowley, Andrea Ballabio, Joel D Schilling, Slava Epelman, Conrad C Weihl, Abhinav Diwan, Daping Fan, Mohamed A Zayed, Babak Razani
Macrophages specialize in removing lipids and debris present in the atherosclerotic plaque. However, plaque progression renders macrophages unable to degrade exogenous atherogenic material and endogenous cargo including dysfunctional proteins and organelles. Here we show that a decline in the autophagy-lysosome system contributes to this as evidenced by a derangement in key autophagy markers in both mouse and human atherosclerotic plaques. By augmenting macrophage TFEB, the master transcriptional regulator of autophagy-lysosomal biogenesis, we can reverse the autophagy dysfunction of plaques, enhance aggrephagy of p62-enriched protein aggregates and blunt macrophage apoptosis and pro-inflammatory IL-1β levels, leading to reduced atherosclerosis...
June 7, 2017: Nature Communications
https://www.readbyqxmd.com/read/28547982/clinicopathological-study-of-5-cases-of-renal-cell-carcinoma-with-t-6-11-p21-q12
#15
Naoto Kuroda, Kenji Yorita, Naomi Sasaki, Akira Ishihara, Keiko Matsuura, Tsutomu Daa, Shintaro Mori, Aya Sasaki, Shuji Mikami, Kazuto Shigematsu, Yoji Nagashima
Renal cell carcinoma (RCC) with t(6;11)(p21;q12) has been incorporated into the recent WHO classification. We performed a clinicopathological study of 5 cases with such a tumor. The patients consisted of 4 males and 1 female. The age of patients ranged from 17 to 57 years with a mean age of 38.6 years. Tumor sizes ranged from 2.8 to 11 cm with a mean value of 6.5 cm. Despite immunotherapy and molecular-targeted therapy, one patient died of the disease 28 months after the surgery. Grossly, the cut surface of this tumor showed grayish white color in at least the focal area of all tumors...
2017: Polish Journal of Pathology: Official Journal of the Polish Society of Pathologists
https://www.readbyqxmd.com/read/28525743/bromodomain-protein-brd4-is-a-transcriptional-repressor-of-autophagy-and-lysosomal-function
#16
Jun-Ichi Sakamaki, Simon Wilkinson, Marcel Hahn, Nilgun Tasdemir, Jim O'Prey, William Clark, Ann Hedley, Colin Nixon, Jaclyn S Long, Maria New, Tim Van Acker, Sharon A Tooze, Scott W Lowe, Ivan Dikic, Kevin M Ryan
Autophagy is a membrane-trafficking process that directs degradation of cytoplasmic material in lysosomes. The process promotes cellular fidelity, and while the core machinery of autophagy is known, the mechanisms that promote and sustain autophagy are less well defined. Here we report that the epigenetic reader BRD4 and the methyltransferase G9a repress a TFEB/TFE3/MITF-independent transcriptional program that promotes autophagy and lysosome biogenesis. We show that BRD4 knockdown induces autophagy in vitro and in vivo in response to some, but not all, situations...
May 18, 2017: Molecular Cell
https://www.readbyqxmd.com/read/28505146/upregulated-autophagy-in-sertoli-cells-of-ethanol-treated-rats-is-associated-with-induction-of-inducible-nitric-oxide-synthase-inos-androgen-receptor-suppression-and-germ-cell-apoptosis
#17
Akio Horibe, Nabil Eid, Yuko Ito, Hitomi Hamaoka, Yoshihisa Tanaka, Yoichi Kondo
This study was conducted to investigate the autophagic response of Sertoli cells (SCs) to acute ethanol toxicity using in vivo and in vitro models. Adult Wistar rats were intraperitoneally injected with either 5 g/kg ethanol or phosphate-buffered saline (for the control group) and sacrificed 0, 3, 6 and 24 h after injection. Compared to the control group, enhanced germ cell apoptosis was observed in the ethanol-treated rats (ETRs) in association with upregulation of iNOS and reduced expression of androgen receptor protein levels in SCs, which were resistant to apoptosis...
May 15, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28483914/tfe3-and-tfeb-transcriptionally-regulate-ppar%C3%AE-2-expression-in-adipocytes-and-mediate-adiponectin-and-glucose-levels-in-mice
#18
Nunciada Salma, Jun S Song, Akinori Kawakami, Suprabha P Devi, Mehdi Khaled, José M Cacicedo, David E Fisher
Members of the MiT transcription factor family are pivotal regulators of several lineage-selective differentiation programs. We show that two of these, Tfeb and Tfe3, control the regulator of adipogenesis, Pparγ2. Knockdown of Tfeb or Tfe3 expression during in vitro adipogenesis causes dramatic downregulation of Pparγ2 expression as well as adipogenesis. Additionally, we found that these factors regulate Pparγ2 in mature adipocytes. Next, we demonstrated that Tfeb and Tfe3 act directly by binding to consensus E-boxes within the Pparγ transcriptional regulatory region...
May 8, 2017: Molecular and Cellular Biology
https://www.readbyqxmd.com/read/28466394/involvement-of-c-abl-kinase-in-microglial-activation-of-nlrp3-inflammasome-and-impairment-in-autolysosomal-system
#19
Vivek Lawana, Neeraj Singh, Souvarish Sarkar, Adhithiya Charli, Huajun Jin, Vellareddy Anantharam, Anumantha G Kanthasamy, Arthi Kanthasamy
A growing body of evidence suggests that excessive microglial activation and pesticide exposure may be linked to the etiology of PD; however, the mechanisms involved remain elusive. Emerging evidence indicates that intracellular inflammasome complex namely NLRP3 complex is involved in the recognition and execution of host inflammatory response. Thus, in the present study, we investigated the hypothesis that NLRP3 inflammasome activation is linked to rotenone (ROT)-induced microglial activation which is dependent upon a priming stimulus by a pathogen-associated molecular pattern (PAMP) or damage associated molecular pattern (DAMP), respectively...
May 2, 2017: Journal of Neuroimmune Pharmacology: the Official Journal of the Society on NeuroImmune Pharmacology
https://www.readbyqxmd.com/read/28465352/cystinosin-the-small-gtpase-rab11-and-the-rab7-effector-rilp-regulate-intracellular-trafficking-of-the-chaperone-mediated-autophagy-receptor-lamp2a
#20
Jinzhong Zhang, Jennifer L Johnson, Jing He, Gennaro Napolitano, Mahalakshmi Ramadass, Celine Rocca, William B Kiosses, Cecilia Bucci, Qisheng Xin, Evripidis Gavathiotis, Ana María Cuervo, Stephanie Cherqui, Sergio D Catz
The lysosomal storage disease cystinosis, caused by cystinosin deficiency, is characterized by cell malfunction, tissue failure, and progressive renal injury despite cystine-depletion therapies. Cystinosis is associated with defects in chaperone-mediated autophagy (CMA), but the molecular mechanisms are incompletely understood. Here, we show CMA substrate accumulation in cystinotic kidney proximal tubule cells. We also found mislocalization of the CMA lysosomal receptor LAMP2A and impaired substrate translocation into the lysosome caused by defective CMA in cystinosis...
June 23, 2017: Journal of Biological Chemistry
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