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https://www.readbyqxmd.com/read/28109117/lipid-profiling-of-parkin-mutant-human-skin-fibroblasts
#1
Simona Lobasso, Paola Tanzarella, Daniele Vergara, Michele Maffia, Tiziana Cocco, Angela Corcelli
Parkin mutations are a major cause of early-onset Parkinson's disease (PD). The impairment of protein quality control system together with defects in mitochondria and autophagy process are consequences of the lack of parkin, which leads to neurodegeneration. Little is known about the role of lipids in these alterations of cell functions. In the present study parkin-mutant human skin primary fibroblasts have been considered as cellular model of PD to investigate on possible lipid alterations associated with the lack of parkin protein...
January 21, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28108329/exercise-increases-mitochondrial-complex-i-activity-and-drp1-expression-in-the-brains-of-aged-mice
#2
Aaron M Gusdon, Jason Callio, Giovanna DiStefano, Robert M O'Doherty, Bret H Goodpaster, Paul M Coen, Charleen T Chu
Exercise is known to have numerous beneficial effects. Recent studies indicate that exercise improves mitochondrial energetics not only in skeletal muscle but also in other tissues. While exercise elicits positive effects on memory, neurogenesis, and synaptic plasticity, the effects of exercise on brain mitochondrial energetics remain relatively unknown. Herein, we studied the effects of exercise training in old and young mice on brain mitochondrial energetics, in comparison to known effects on peripheral tissues that utilize fatty acid oxidation...
January 17, 2017: Experimental Gerontology
https://www.readbyqxmd.com/read/28108310/autophagic-dysregulation-in-doxorubicin-cardiomyopathy
#3
REVIEW
Jordan J Bartlett, Purvi C Trivedi, Thomas Pulinilkunnil
Doxorubicin (DOX)-induced cardiotoxicity has been a well-known phenomenon to clinicians and scientists for decades; however, molecular mechanisms underlying DOX cardiotoxicity are still being uncovered. Although prior research has mostly implicated disruptive events in the nucleus and mitochondria to be contributing to DOX cardiomyopathy, recent discoveries in the cellular waste management process, autophagy, have highlighted the role of the lysosome, an organelle central to autophagy, in this pathology. Indeed, dysregulation of lysosomal autophagy is observed in pre-clinical models of DOX cardiotoxicity...
January 17, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28106298/inhibition-of-inositol-1-4-5-trisphosphate-receptor-induce-breast-cancer-cell-death-through-deregulated-autophagy-and-cellular-bioenergetics
#4
Aru Singh, Megha Chagtoo, Swasti Tiwari, Nelson George, Bandana Chakravarti, Sajid Khan, Sripada Lakshmi, Madan M Godbole
Inositol 1,4,5-trisphosphate receptors (IP3 Rs) regulate autophagy in normal cells and are associated with metastasis in cancer cells. In breast cancer, however, the regulation and role of IP3 Rs is not clear. To study this we used MCF-7 breast cancer cell line and mouse model of breast cancer. Inhibiting IP3 R sub types resulted in compromised bioenergetics both in terms of glucose and mitochondrial metabolism. The siRNA mediated silencing of IP3 R or its blocking by its inhibitors Xestospongin C and 2-Amino-ethoxy diphenyl borate increased cell death and LC3II expression in MCF-7 cells as well as attenuated cellular bioenergetics...
January 20, 2017: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/28104670/mutants-for-drosophila-isocitrate-dehydrogenase-3b-are-defective-in-mitochondrial-function-and-larval-cell-death
#5
Dianne M Duncan, Paula Kiefel, Ian Duncan
The death of larval salivary gland cells during metamorphosis in Drosophila melanogaster has been a key system for studying steroid controlled programmed cell death. This death is induced by a pulse of the steroid hormone ecdysone that takes place at the end of the prepupal period. For many years, it has been thought that the ecdysone direct response gene Eip93F (E93) plays a critical role in initiating salivary gland cell death. This conclusion was based largely on the finding that the three "type" alleles of E93 cause a near-complete block in salivary gland cell death...
January 18, 2017: G3: Genes—Genomes—Genetics
https://www.readbyqxmd.com/read/28103798/selenium-suppresses-glutamate-induced-cell-death-and-prevents-mitochondrial-morphological-dynamic-alterations-in-hippocampal-ht22-neuronal-cells
#6
Yan-Mei Ma, Gordon Ibeanu, Li-Yao Wang, Jian-Zhong Zhang, Yue Chang, Jian-Da Dong, P Andy Li, Li Jing
BACKGROUND: Previous studies have indicated that selenium supplementation may be beneficial in neuroprotection against glutamate-induced cell damage, in which mitochondrial dysfunction is considered a major pathogenic feature. However, the exact mechanisms by which selenium protects against glutamate-provoked mitochondrial perturbation remain ambiguous. In this study glutamate exposed murine hippocampal neuronal HT22 cell was used as a model to investigate the underlying mechanisms of selenium-dependent protection against mitochondria damage...
January 19, 2017: BMC Neuroscience
https://www.readbyqxmd.com/read/28103115/involvement-of-autophagy-in-nk-cell-development-and-function
#7
Alejandro López-Soto, José Manuel Bravo-San Pedro, Guido Kroemer, Lorenzo Galluzzi, Segundo Gonzalez
Natural killer (NK) cells are the prototypical members of the recently identified family of innate lymphoid cells (ILCs). Thanks to their cytotoxic and secretory functions, NK cells play a key role in the immune response to cells experiencing various forms of stress, including viral infection and malignant transformation. Autophagy is a highly conserved network of degradative pathways that participate in the maintenance of cellular and organismal homeostasis as they promote adaptation to adverse microenvironmental conditions...
January 19, 2017: Autophagy
https://www.readbyqxmd.com/read/28102843/il-17-mediated-mitochondrial-dysfunction-impairs-apoptosis-in-rheumatoid-arthritis-synovial-fibroblasts-through-activation-of-autophagy
#8
Eun Kyung Kim, Jeong-Eun Kwon, Seon-Young Lee, Eun-Jung Lee, Da Som Kim, Su-Jin Moon, Jennifer Lee, Seung-Ki Kwok, Sung-Hwan Park, Mi-La Cho
Fibroblast-like synoviocytes (FLSs) are a major cell population of the pannus that invades cartilage and bone in rheumatoid arthritis (RA). FLS resistance to apoptosis is a major characteristic of RA. The aims of this study were to investigate the effects of interleukin-17 (IL-17) and IL-17-producing T helper (Th17) cells on resistance to apoptosis in FLSs from RA patients (RA FLSs) and their roles in mitochondrial dysfunction and autophagy. Mitochondrial function was assessed in RA FLSs and FLSs from osteoarthritis patients (OA FLSs)...
January 19, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28093052/erk-nrf2-ho-1-pathway-mediated-mitophagy-alleviates-traumatic-brain-injury-induced-intestinal-mucosa-damage-and-epithelial-barrier-dysfunction
#9
Yinlong Liu, Zhongyuan Bao, Xiupeng Xu, Honglu Chao, Chao Lin, Zheng Li, Yan Liu, Xiaoming Wang, Yongping You, Ning Liu, Jing Ji
Gastrointestinal dysfunction is one of several physiologic complications in patients with traumatic brain injury (TBI). TBI can result in increased intestinal permeability due to apoptosis of intestinal epithelial cells, which contain a large number of mitochondria for persisting barrier function. Autophagy of damaged mitochondria (mitophagy) controls the quality of the mitochondria and regulates cellular homeostasis. However, the exact mechanism of mitophagy that underlies the pathological changes induced by TBI is unknown...
January 16, 2017: Journal of Neurotrauma
https://www.readbyqxmd.com/read/28092677/wnt-%C3%AE-catenin-signaling-regulates-mitochondrial-activity-to-alter-the-oncogenic-potential-of-melanoma-in-a-pten-dependent-manner
#10
K Brown, P Yang, D Salvador, R Kulikauskas, H Ruohola-Baker, A M Robitaille, A J Chien, R T Moon, V Sherwood
Aberrant regulation of WNT/β-catenin signaling has a crucial role in the onset and progression of cancers, where the effects are not always predictable depending on tumor context. In melanoma, for example, models of the disease predict differing effects of the WNT/β-catenin pathway on metastatic progression. Understanding the processes that underpin the highly context-dependent nature of WNT/β-catenin signaling in tumors is essential to achieve maximal therapeutic benefit from WNT inhibitory compounds. In this study, we have found that expression of the tumor suppressor, phosphatase and tensin homolog deleted on chromosome 10 (PTEN), alters the invasive potential of melanoma cells in response to WNT/β-catenin signaling, correlating with differing metabolic profiles...
January 16, 2017: Oncogene
https://www.readbyqxmd.com/read/28089824/mitochondrial-uncoupling-protein-2-in-human-cumulus-cells-is-associated-with-regulating-autophagy-and-apoptosis-maintaining-gap-junction-integrity-and-progesterone-synthesis
#11
Hongshan Ge, Fan Zhang, Duan Ping, Nan Zhu, Jiayan Zhang, Feijun Ye, Dan Shan, Hua Chen, XiaoSheng Lu, ChunFang Zhu, Renshan Ge, Zhenkun Lin
To explore the roles of mitochondrial Uncoupling Protein 2 (UCP2) in cumulus cells (CCs), human CCs were cultured in vitro, and the UCP2 was inhibited by treatment with Genipin, a special UCP inhibitor, or by RNA interference targeting UCP2. No significant differences in adenosine triphosphate levels and the ratio of ADP/ATP were observed after UCP2 inhibition. UCP2 inhibition caused a significant increase in cellular oxidative damage, which was reflected in alterations to several key parameters, including reactive oxygen species (ROS) and lipid peroxidation levels and the ratio of reduced GSH to GSSG...
January 12, 2017: Molecular and Cellular Endocrinology
https://www.readbyqxmd.com/read/28088622/reactive-oxygen-species-and-cancer-paradox-to-promote-or-to-suppress
#12
REVIEW
Sehamuddin Galadari, Anees Rahman, Siraj Pallichankandy, Faisal Thayyullathil
Reactive oxygen species (ROS), a group of highly reactive ions and molecules, are increasingly being appreciated as powerful signaling molecules involved in the regulation of a variety of biological processes. Indeed, their role is continuously being delineated in a variety of pathophysiological conditions. For instance, cancer cells are shown to have increased ROS levels in comparison to their normal counterparts. This is partly due to an enhanced metabolism and mitochondrial dysfunction in cancer cells. The escalated ROS generation in cancer cells contributes to the biochemical and molecular changes necessary for the tumor initiation, promotion and progression, as well as, tumor resistance to chemotherapy...
January 11, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28087295/postconditioning-induced-neuroprotection-mechanisms-and-applications-in-cerebral-ischemia
#13
REVIEW
Yan-Ying Fan, Wei-Wei Hu, Fang Nan, Zhong Chen
Ischemic postconditioning (PostC) is defined as a series of rapid intermittent interruptions of blood flow at the phase of reperfusion, which produces neuroprotection against cerebral ischemia/reperfusion injury via mobilizing the brain's own endogenous adaptive mechanisms. Now the concept of conventional ischemic PostC has been extended to limb remote ischemic PostC and chemical PostC with hypoxia, volatile anesthetic, CO2, etc. According to the different temporal profile of PostC, it is divided into rapid and delayed PostC...
January 10, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28076378/p62-pathology-model-in-the-rat-substantia-nigra-with-filamentous-inclusions-and-progressive-neurodegeneration
#14
Kasey L Jackson, Wen-Lang Lin, Sumitra Miriyala, Robert D Dayton, Manikandan Panchatcharam, Kevin J McCarthy, Monica Castanedes-Casey, Dennis W Dickson, Ronald L Klein
One of the proteins most frequently found in neuropathological lesions is the ubiquitin binding protein p62 (sequestosome 1). Post-mortem analysis of p62 is a defining diagnostic marker in several neurodegenerative diseases including amyotrophic lateral sclerosis and inclusion body myositis. Since p62 functions in protein degradation pathways including autophagy, the build-up of p62-positive inclusions suggests defects in protein clearance. p62 was expressed unilaterally in the rat substantia nigra with an adeno-associated virus vector (AAV9) in order to study p62 neuropathology...
2017: PloS One
https://www.readbyqxmd.com/read/28069524/atg14-facilitated-lipophagy-in-cancer-cells-induce-er-stress-mediated-mitoptosis-through-a-ros-dependent-pathway
#15
Subhadip Mukhopadhyay, Isabel R Schlaepfer, Bryan C Bergman, Prashanta Kumar Panda, Prakash Priyadarshi Praharaj, Prajna Paramita Naik, Rajesh Agarwal, Sujit Kumar Bhutia
Understanding the dynamics of autophagy and apoptosis crosstalk in cancer progression remains a challenging task. Here, we reported how the autophagy protein ATG14 induces lipophagy-mediated mitochondrial apoptosis. The overexpression of ATG14 in HeLa cells inhibited cell viability and increased mitochondrial apoptosis and endoplasmic reticulum (ER) stress. Furthermore, inhibition of this ATG14-induced autophagy promoted apoptosis. ATG14 overexpression resulted in the accumulation of stearic acid and oleic acid free fatty acids (FFA), with a concomitant decrease in the number of lipid droplets...
January 6, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28068143/adaptations-to-excess-choline-in-insulin-resistant-and-pcyt2-deficient-skeletal-muscle
#16
Adrian Taylor, Laila Cigana Schenkel, Maiya Yokich, Marica Bakovic
It was hypothesized that choline supplementation in insulin resistant (IR) CTP:phosphoethanolamine cytidylyltransferase deficient (Pcyt2(+/-)) mice would ameliorate muscle function by remodeling glucose and fatty acid (FA) metabolism. Pcyt2(+/-) mice either received no treatment or were allowed access to 2 mg/mL choline in drinking water for 4 weeks. Skeletal muscle was harvested from choline treated and untreated mice. Lipid analysis and metabolic gene expression and signaling pathways were compared between untreated Pcyt2(+/-) mice, treated Pcyt2(+/-) mice, and Pcyt2(+/+) mice...
September 6, 2016: Biochemistry and Cell Biology, Biochimie et Biologie Cellulaire
https://www.readbyqxmd.com/read/28066797/mitochondrial-dysfunction-activates-the-ampk-signaling-and-autophagy-to-promote-cell-survival
#17
Baozhong Zhao, Lei Qiang, Joy Joseph, Balaraman Kalyanaraman, Benoit Viollet, Yu-Ying He
Autophagy is a cellular self-eating process essential for stress response and maintaining tissue homeostasis by lysosomal degradation of unwanted or damaged proteins and organelles. Here, we show that cells with defective mitochondria induce autophagy to promote cell survival through activating the AMPK pathway. Loss of mitochondrial complex III protein cytochrome b activates the AMPK signaling and induced autophagy. Inhibiting mitochondria energetics by mitochondria-targeted agents activates the AMPK signaling and induced autophagy...
March 2016: Genes & Diseases
https://www.readbyqxmd.com/read/28062576/cardiolipin-regulates-mitophagy-through-the-pkc-pathway
#18
Zheni Shen, Yiran Li, Alexander N Gasparski, Hagai Abeliovich, Miriam L Greenberg
Cardiolipin (CL), the signature phospholipid of mitochondrial membranes, is important for cardiovascular health, and perturbation of CL metabolism is implicated in cardiovascular disease (CVD). While the role of CL in mitochondrial function, biogenesis, and genome stability has been studied, recent findings indicate that it is essential for functions apart from mitochondrial bioenergetics. In this study, we report that mitophagy is perturbed in CL deficient yeast cells. Mutants of autophagy/mitophagy genes ATG8, ATG18 and ATG32 synthetically interact with CL synthase mutant crd1Δ CL-deficient cells exhibited decreased GFP-tagged mitochondrial proteins inside the vacuole and decreased free GFP, consistent with decreased mitophagy...
January 5, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28060865/agent-based-modeling-of-mitochondria-links-sub-cellular-dynamics-to-cellular-homeostasis-and-heterogeneity
#19
Giovanni Dalmasso, Paula Andrea Marin Zapata, Nathan Ryan Brady, Anne Hamacher-Brady
Mitochondria are semi-autonomous organelles that supply energy for cellular biochemistry through oxidative phosphorylation. Within a cell, hundreds of mobile mitochondria undergo fusion and fission events to form a dynamic network. These morphological and mobility dynamics are essential for maintaining mitochondrial functional homeostasis, and alterations both impact and reflect cellular stress states. Mitochondrial homeostasis is further dependent on production (biogenesis) and the removal of damaged mitochondria by selective autophagy (mitophagy)...
2017: PloS One
https://www.readbyqxmd.com/read/28057766/rapid-degradation-of-mutant-slc25a46-by-the-ubiquitin-proteasome-system-results-in-mfn1-2-mediated-hyperfusion-of-mitochondria
#20
Janos Steffen, Ajay A Vashisht, Jijun Wan, Joanna C Jen, Steven M Claypool, James A Wohlschlegel, Carla M Koehler
SCL25A46 is a member of the mitochondrial carrier protein that surprisingly localizes to the outer membrane and is distantly related to Ugo1. Here we show that a subset of SLC25A46 interacted with mitochondrial dynamics components and the MICOS complex. Decreased expression of SLC25A46 resulted in increased stability and oligomerization of MFN1 and MFN2 on mitochondria, promoting mitochondrial hyperfusion. A mutation at L341P caused rapid degradation of SLC25A46 that manifested as a rare disease, pontocerebellar hypoplasia...
January 5, 2017: Molecular Biology of the Cell
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