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Mitochondria AND mTOR

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https://www.readbyqxmd.com/read/27913682/translational-regulation-of-mitochondrial-biogenesis
#1
REVIEW
Yi Zhang, Hong Xu
Mitochondria are generated by the expression of genes on both nuclear and mitochondrial genome. Mitochondrial biogenesis is highly plastic in response to cellular energy demand, developmental signals and environmental stimuli. Mechanistic target of rapamycin (mTOR) pathway regulates mitochondrial biogenesis to co-ordinate energy homeostasis with cell growth. The local translation of mitochondrial proteins on the outer membrane facilitates their efficient import and thereby allows prodigious mitochondrial biogenesis during rapid cell growth and proliferation...
December 15, 2016: Biochemical Society Transactions
https://www.readbyqxmd.com/read/27913603/the-tumor-suppressor-flcn-mediates-an-alternate-mtor-pathway-to-regulate-browning-of-adipose-tissue
#2
Shogo Wada, Michael Neinast, Cholsoon Jang, Yasir H Ibrahim, Gina Lee, Apoorva Babu, Jian Li, Atsushi Hoshino, Glenn C Rowe, James Rhee, José A Martina, Rosa Puertollano, John Blenis, Michael Morley, Joseph A Baur, Patrick Seale, Zoltan Arany
Noncanonical mechanistic target of rapamycin (mTOR) pathways remain poorly understood. Mutations in the tumor suppressor folliculin (FLCN) cause Birt-Hogg-Dubé syndrome, a hamartomatous disease marked by mitochondria-rich kidney tumors. FLCN functionally interacts with mTOR and is expressed in most tissues, but its role in fat has not been explored. We show here that FLCN regulates adipose tissue browning via mTOR and the transcription factor TFE3. Adipose-specific deletion of FLCN relieves mTOR-dependent cytoplasmic retention of TFE3, leading to direct induction of the PGC-1 transcriptional coactivators, drivers of mitochondrial biogenesis and the browning program...
December 2, 2016: Genes & Development
https://www.readbyqxmd.com/read/27897419/exercise-restores-muscle-stem-cell-mobilization-regenerative-capacity-and-muscle-metabolic-alterations-via-adiponectin-adipor1-activation-in-samp10-mice
#3
Aiko Inoue, Xian Wu Cheng, Zhe Huang, Lina Hu, Ryosuke Kikuchi, Haiying Jiang, Limei Piao, Takeshi Sasaki, Kohji Itakura, Hongxian Wu, Guangxian Zhao, Yanna Lei, Guang Yang, Enbo Zhu, Xiang Li, Kohji Sato, Teruhiko Koike, Masafumi Kuzuya
BACKGROUND: Exercise train (ET) stimulates muscle response in pathological conditions, including aging. The molecular mechanisms by which exercise improves impaired adiponectin/adiponectin receptor 1 (AdipoR1)-related muscle actions associated with aging are poorly understood. Here we observed that in a senescence-accelerated mouse prone 10 (SAMP10) model, long-term ET modulated muscle-regenerative actions. METHODS: 25-week-old male SAMP10 mice were randomly assigned to the control and the ET (45 min/time, 3/week) groups for 4 months...
November 29, 2016: Journal of Cachexia, Sarcopenia and Muscle
https://www.readbyqxmd.com/read/27888070/phosphoramide-mustard-induces-autophagy-markers-and-mtor-inhibition-prevents-follicle-loss-due-to-phosphoramide-mustard-exposure
#4
Jill A Madden, Porsha Q Thomas, Aileen F Keating
Phosphoramide mustard (PM) is an ovotoxic metabolite of cyclophosphamide. Postnatal day 4 Fisher 344 rat ovaries were exposed to vehicle control (1% DMSO) or PM (60μM)±LY294002 or rapamycin for 2 or 4 d. Transmission election microscopy revealed abnormally large golgi apparatus and electron dense mitochondria in PM-exposed ovaries prior to and at the time of follicle depletion. PM exposure increased (P<0.05) mRNA abundance of Bbc3, Cdkn1a, Ctfr, Edn1, Gstp1, Nqo1, Tlr4, Tnfrsfla, Txnrd1 and decreased (P<0...
November 22, 2016: Reproductive Toxicology
https://www.readbyqxmd.com/read/27865838/helix-b-surface-peptide-attenuates-diabetic-cardiomyopathy-via-ampk-dependent-autophagy
#5
Chen Lin, Mingming Zhang, Yingmei Zhang, Kejian Yang, Jianqiang Hu, Rui Si, Guoyong Zhang, Beilei Gao, Xiang Li, Chennian Xu, Congye Li, Qimeng Hao, Wenyi Guo
BACKGROUND: Erythropoietin (EPO) has been reported to exert protective effects on a host of damaged tissues. However, the erythropoietic effect of this hormone can result in high risks of thrombosis, stroke, and hypertension, remarkably limiting the clinical use of EPO. Helix B surface peptide (HBSP) is a small peptide derived from the helix-B domain of EPO. Surprisingly, HBSP retains the tissue protective properties of EPO without altering the hematocrit. Thus, we evaluated the possible role of HBSP on diabetic cardiomyopathy...
November 16, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27863407/induction-of-mitochondria-mediated-apoptosis-and-pi3k-akt-mtor-mediated-autophagy-by-aflatoxin-b2-in-hepatocytes-of-broilers
#6
Binlong Chen, Diyan Li, Miao Li, Sichen Li, Kenan Peng, Xian Shi, Lanyun Zhou, Pu Zhang, Zhongxian Xu, Huadong Yin, Yan Wang, Xiaoling Zhao
Aflatoxins have been shown to induce hepatotoxicity in animal models, but the effects of aflatoxin B2 (AFB2) on broiler hepatocytes is unclear. This study aimed to investigate the effects of AFB2 on apoptosis and autophagy to provide an experimental basis for understanding the mechanism of aflatoxin-induced hepatotoxicity. One hundred-twenty Cobb500 broilers were allocated to four groups and exposed to 0 mg/kg, 0.2 mg/kg, 0.4 mg/kg, and 0.8 mg/kg of AFB2 per day for 21 d. AFB2 exerted potent proapoptotic and proautophagic effects on hepatocytes, with increased numbers of apoptotic and autophagic hepatocytes...
November 15, 2016: Oncotarget
https://www.readbyqxmd.com/read/27849558/identification-of-a-fluorescent-small-molecule-enhancer-for-therapeutic-autophagy-in-colorectal-cancer-by-targeting-mitochondrial-protein-translocase-tim44
#7
Yinghui Huang, Jie Zhou, Shenglin Luo, Yang Wang, Jintao He, Peng Luo, Zelin Chen, Tao Liu, Xu Tan, Juanjuan Ou, Hongming Miao, Houjie Liang, Chunmeng Shi
OBJECTIVE: As the modulation of autophagic processes can be therapeutically beneficial to cancer treatment, the identification of novel autophagic enhancers is highly anticipated. However, current autophagy-inducing anticancer agents exert undesired side effects owing to their non-specific biodistribution in off-target tissues. This study aims to develop a multifunctional agent to integrate cancer targeting, imaging and therapy and to investigate its mechanism. DESIGN: A series of mitochondria-targeting near-infrared (NIR) fluorophores were synthesised, screened and identified for their autophagy-enhancing activity...
November 14, 2016: Gut
https://www.readbyqxmd.com/read/27831748/therapeutic-effects-of-antibiotic-drug-mefloquine-against-cervical-cancer-through-impairing-mitochondrial-function-and-inhibiting-mtor-pathway
#8
Hui Li, Shun Jiao, Xin Li, Hasina Banu, Shreejana Hamal, Xianrong Wang
Targeting mitochondria is an attractive strategy for cancer therapy due to the essential roles of mitochondria in cancer cell energy metabolism. In this study, we show that mefloquine, an antibiotic drug, effectively targets cervical cancer cells through impairing mitochondrial function. Mefloquine dose-dependently induces apoptosis and inhibits proliferation and anchorage-independent colony formation of multiple cervical cancer cell lines. Mefloquine alone inhibits cervical tumor growth in vivo and its combination with paclitaxel is synergistic in inhibiting tumor growth...
August 11, 2016: Canadian Journal of Physiology and Pharmacology
https://www.readbyqxmd.com/read/27817185/pharmacologic-inhibition-of-autophagy-sensitizes-human-acute-leukemia-jurkat-t-cells-to-acacetin-induced-apoptosis
#9
Ji Young Lee, Do Youn Jun, Ki Yun Kim, Eun Ji Ha, Mi Hee Woo, Jee Youn Ko, Young Ho Yun, In-Seok Oh, Young Ho Kim
Exposure of Jurkat T cell clone (J/Neo cells) to acacetin (5,7-dihydroxy-4'-methoxyflavone), which is present in barnyard millet [Echinochloa esculenta (A. Braun)] grains, resulted in cytotoxicity, accumulation of apoptotic sub-G1 cells, Bak activation, loss of mitochondrial membrane potential (Δψm), activation of caspase-9 and caspase-3, cleavage of poly (ADP-ribose) polymerase (PARP), and FITC-Annexin V-stainable phosphatidylserine exposure on the external surface of the cytoplasmic membrane without accompanying necrosis...
November 4, 2016: Journal of Microbiology and Biotechnology
https://www.readbyqxmd.com/read/27815218/oxyresveratrol-activates-parallel-apoptotic-and-autophagic-cell-death-pathways-in-neuroblastoma-cells
#10
Md Ataur Rahman, Kausik Bishayee, Ali Sadra, Sung-Oh Huh
BACKGROUND: Drug resistance from apoptosis is a challenging issue with different cancer types, and there is an interest in identifying other means of inducing cytotoxicity. Here, treatment of neuroblastoma cells with oxyresveratrol (OXYRES), a natural antioxidant, led to dose-dependent cell death and increased autophagic flux along with activation of caspase-dependent apoptosis. METHODS: For cell viability, we performed the CCK-8 assay. Protein expression changes were with Western blot and immunocytochemistry...
November 2, 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27814983/endosulfan-induces-autophagy-and-endothelial-dysfunction-via-the%C3%A2-ampk-mtor-signaling-pathway-triggered-by-oxidative-stress
#11
Lianshuang Zhang, Jialiu Wei, Lihua Ren, Jin Zhang, Ji Wang, Li Jing, Man Yang, Yang Yu, Zhiwei Sun, Xianqing Zhou
Cardiovascular diseases is related to environmental pollution. Endosulfan is an organochlorine pesticide and its toxicity has been reported. However, the relationship between oxidative stress and autophagy induced by endosulfan and its underlying mechanism remain confusing. In this study, human umbilical vein endothelial cells (HUVECs) were chosen to explore the toxicity mechanism and were treated with 0, 1, 6, 12 μg/mL(-1) endosulfan for 24 h, respectively. The present results showed that autophagy could be induced by endosulfan, which was verified by the monodansylcadaverine staining, autophagic ultrastructural observation, and LC3-I/LC3-II conversion...
January 2017: Environmental Pollution
https://www.readbyqxmd.com/read/27793977/acute-stimulation-of-glucose-influx-upon-mitoenergetic-dysfunction-requires-lkb1-ampk-sirt2-and-mtor-raptor
#12
Dania C Liemburg-Apers, Jori A L Wagenaars, Jan A M Smeitink, Peter H G M Willems, Werner J H Koopman
Mitochondria play a central role in cellular energy production, and their dysfunction can trigger a compensatory increase in glycolytic flux to sustain cellular ATP levels. Here, we studied the mechanism of this homeostatic phenomenon in C2C12 myoblasts. Acute (30 min) mitoenergetic dysfunction induced by the mitochondrial inhibitors piericidin A and antimycin A stimulated Glut1-mediated glucose uptake without altering Glut1 (also known as SLC2A1) mRNA or plasma membrane levels. The serine/threonine liver kinase B1 (LKB1; also known as STK11) and AMP-activated protein kinase (AMPK) played a central role in this stimulation...
December 1, 2016: Journal of Cell Science
https://www.readbyqxmd.com/read/27791464/autophagy-impairment-with-lysosomal-and-mitochondrial-dysfunction-is-an-important-characteristic-of-oxidative-stress-induced-senescence
#13
Haoran Tai, Zhe Wang, Hui Gong, Xiaojuan Han, Jiao Zhou, Xiaobo Wang, Xiawei Wei, Yi Ding, Ning Huang, Jianqiong Qin, Jie Zhang, Shuang Wang, Fei Gao, Zofia M Chrzanowska-Lightowlers, Rong Xiang, Hengyi Xiao
Macroautophagy/autophagy has profound implications for aging. However, the true features of autophagy in the progression of aging remain to be clarified. In the present study, we explored the status of autophagic flux during the development of cell senescence induced by oxidative stress. In this system, although autophagic structures increased, the degradation of SQSTM1/p62 protein, the yellow puncta of mRFP-GFP-LC3 fluorescence and the activity of lysosomal proteolytic enzymes all decreased in senescent cells, indicating impaired autophagic flux with lysosomal dysfunction...
October 28, 2016: Autophagy
https://www.readbyqxmd.com/read/27777385/decreased-mtor-signalling-reduces-mitochondrial-ros-in-brain-via-accumulation-of-the-telomerase-protein-tert-within-mitochondria
#14
Satomi Miwa, Rafal Czapiewski, Tengfei Wan, Amy Bell, Kirsten N Hill, Thomas von Zglinicki, Gabriele Saretzki
Telomerase in its canonical function maintains telomeres in dividing cells. In addition, the telomerase protein TERT has non-telomeric functions such as shuttling to mitochondria resulting in a decreased oxidative stress, DNA damage and apoptosis. TERT protein persists in adult neurons and can co-localise to mitochondria under various stress conditions. We show here that TERT expression decreased in mouse brain during aging while release of reactive oxygen species (ROS) from the mitochondrial electron transport chain increased...
October 22, 2016: Aging
https://www.readbyqxmd.com/read/27771251/anthelmintic-drug-ivermectin-inhibits-angiogenesis-growth-and-survival-of-glioblastoma-through-inducing-mitochondrial-dysfunction-and-oxidative-stress
#15
Yingying Liu, Shanshan Fang, Qiushi Sun, Bo Liu
Glioblastoma is one of the most vascular brain tumour and highly resistant to current therapy. Targeting both glioblastoma cells and angiogenesis may present an effective therapeutic strategy for glioblastoma. In our work, we show that an anthelmintic drug, ivermectin, is active against glioblastoma cells in vitro and in vivo, and also targets angiogenesis. Ivermectin significantly inhibits growth and anchorage-independent colony formation in U87 and T98G glioblastoma cells. It induces apoptosis in these cells through a caspase-dependent manner...
October 19, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27760377/therapeutic-relevance-of-mtor-inhibition-in-murine-succinate-semialdehyde-dehydrogenase-deficiency-ssadhd-a-disorder-of-gaba-metabolism
#16
K R Vogel, G R Ainslie, E E W Jansen, G S Salomons, K M Gibson
Aldehyde dehydrogenase 5a1-deficient (aldh5a1(-/-)) mice, the murine orthologue of human succinic semialdehyde dehydrogenase deficiency (SSADHD), manifest increased GABA (4-aminobutyric acid) that disrupts autophagy, increases mitochondria number, and induces oxidative stress, all mitigated with the mTOR (mechanistic target of rapamycin) inhibitor rapamycin [1]. Because GABA regulates mTOR, we tested the hypothesis that aldh5a1(-/-) mice would show altered levels of mRNA for genes associated with mTOR signaling and oxidative stress that could be mitigated by inhibiting mTOR...
October 17, 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27760312/impaired-mitochondrial-dynamics-and-mitophagy-in-neuronal-models-of-tuberous-sclerosis-complex
#17
Darius Ebrahimi-Fakhari, Afshin Saffari, Lara Wahlster, Alessia Di Nardo, Daria Turner, Tommy L Lewis, Christopher Conrad, Jonathan M Rothberg, Jonathan O Lipton, Stefan Kölker, Georg F Hoffmann, Min-Joon Han, Franck Polleux, Mustafa Sahin
Tuberous sclerosis complex (TSC) is a neurodevelopmental disease caused by TSC1 or TSC2 mutations and subsequent activation of the mTORC1 kinase. Upon mTORC1 activation, anabolic metabolism, which requires mitochondria, is induced, yet at the same time the principal pathway for mitochondrial turnover, autophagy, is compromised. How mTORC1 activation impacts mitochondrial turnover in neurons remains unknown. Here, we demonstrate impaired mitochondrial homeostasis in neuronal in vitro and in vivo models of TSC...
October 18, 2016: Cell Reports
https://www.readbyqxmd.com/read/27748893/crosstalk-between-autophagy-and-intracellular-radiation-response-review
#18
Lelin Hu, Hao Wang, Li Huang, Yong Zhao, Junjie Wang
Autophagy induced by radiation is critical to cell fate decision. Evidence now sheds light on the importance of autophagy induced by cancer radiotherapy. Traditional view considers radiation can directly or indirectly damage DNA which can activate DNA damage the repair signaling pathway, a large number of proteins participating in DNA damage repair signaling pathway such as p53, ATM, PARP1, FOXO3a, mTOR and SIRT1 involved in autophagy regulation. However, emerging recent evidence suggests radiation can also cause injury to extranuclear targets such as plasma membrane, mitochondria and endoplasmic reticulum (ER) and induce accumulation of ceramide, ROS, and Ca2+ concentration which activate many signaling pathways to modulate autophagy...
October 5, 2016: International Journal of Oncology
https://www.readbyqxmd.com/read/27744450/combination-of-hydroxyl-acetylated-curcumin-and-ultrasound-induces-macrophage-autophagy-with-anti-apoptotic-and-anti-lipid-aggregation-effects
#19
Longbin Zheng, Ying Li, Xuesong Li, Jiayuan Kou, Zhaoyu Zhong, Yueqing Jiang, Zhongni Liu, Ye Tian, Liming Yang
BACKGROUND/AIMS: Sonodynamic therapy (SDT) is considered a new approach for the treatment of atherosclerosis. We previously confirmed that hydroxyl acetylated curcumin (HAC) was a sonosensitizer. In this study, we investigated the mechanism of THP-1 macrophage apoptosis and autophagy induced by HAC mediated SDT (HAC-SDT). METHODS: Cell viability was measured using a CCK-8 assay. Laser scanning confocal microscopy was used to measure the levels of intracellular reactive oxygen species (ROS), sub-cellular HAC localization, BAX and cytochrome C translocation, LC3 expression, monodansylcadaverine staining and Dil-labeled oxidized low density lipoprotein (Dil-ox-LDL) uptake...
October 17, 2016: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/27721400/physical-interaction-of-estrogen-receptor-with-mnsod-implication-in-mitochondrial-o2-upregulation-and-mtorc2-potentiation-in-estrogen-responsive-breast-cancer-cells
#20
M-U-D Lone, K S Baghel, R K Kanchan, R Shrivastava, S A Malik, B N Tewari, C Tripathi, M P S Negi, V K Garg, M Sharma, M L B Bhatt, S Bhadauria
Augmented reactive oxygen species levels consequential to functional alteration of key mitochondrial attributes contribute to carcinogenesis, either directly via oxidative DNA damage infliction or indirectly via activation of oncogenic signaling cascades. We previously reported activation of a key oncogenic signaling cascade via mammalian target of rapamycin (mTOR) signaling complex-2 (mTORC2) owing to estrogen receptor (ER-α)-dependent augmentation of O2(.-) within the mitochondria of 17-β-estradiol (E2)-stimulated breast cancer cells...
October 10, 2016: Oncogene
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