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https://www.readbyqxmd.com/read/29046298/identification-of-dual-mechanisms-mediating-5-hydroxytryptamine-receptor-1f-induced-mitochondrial-biogenesis
#1
Whitney S Gibbs, Sara M Garrett, Craig C Beeson, Rick G Schnellmann
Our laboratory recently made the novel observation that 5-hydroxytryptamine 1F (5-HT1F) receptor activation induces mitochondrial biogenesis (MB), the production of new, functional mitochondria, in vitro and vivo. We sought to determine the mechanism linking the 5-HT1F receptor to MB in renal proximal tubule cells. Using LY344864, a selective 5-HT1F receptor agonist, we determined that the 5-HT1F receptor is coupled to Gαi/o and induces MB through Gβγ dependent activation of Akt, endothelial nitric oxide (eNOS), cyclic guanosine-monophosphate (cGMP), protein kinase G (PKG) and peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α)...
October 18, 2017: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/29046293/exercise-induces-tfeb-expression-and-activity-in-skeletal-muscle-in-a-pgc-1%C3%AE-dependent-manner
#2
Avigail T Erlich, Diane M Brownlee, Kaitlyn Beyfuss, David A Hood
The mitochondrial network in muscle is controlled by the opposing processes of mitochondrial biogenesis and mitophagy. The coactivator PGC-1α regulates biogenesis, while the transcription of mitophagy-related genes is controlled by transcription factor EB (TFEB). PGC-1α activation is induced with exercise, however the effect of exercise on TFEB is not fully known. We investigated the interplay between PGC-1α and TFEB on mitochondria in response to acute contractile activity in C2C12 myotubes, and following exercise in WT and PGC-1α KO mice...
October 18, 2017: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/29042548/human-mesenchymal-stromal-cells-transplanted-into-mice-stimulate-renal-tubular-cells-and-enhance-mitochondrial-function
#3
Luca Perico, Marina Morigi, Cinzia Rota, Matteo Breno, Caterina Mele, Marina Noris, Martino Introna, Chiara Capelli, Lorena Longaretti, Daniela Rottoli, Sara Conti, Daniela Corna, Giuseppe Remuzzi, Ariela Benigni
Mesenchymal stromal cells (MSCs) are renoprotective and drive regeneration following injury, although cellular targets of such an effect are still ill-defined. Here, we show that human umbilical cord (UC)-MSCs transplanted into mice stimulate tubular cells to regain mitochondrial mass and function, associated with enhanced microtubule-rich projections that appear to mediate mitochondrial trafficking to create a reparative dialogue among adjacent tubular cells. Treatment with UC-MSCs in mice with cisplatin-induced acute kidney injury (AKI) regulates mitochondrial biogenesis in proximal tubuli by enhancing PGC1α expression, NAD(+) biosynthesis and Sirtuin 3 (SIRT3) activity, thus fostering antioxidant defenses and ATP production...
October 17, 2017: Nature Communications
https://www.readbyqxmd.com/read/29030114/impairment-of-energy-sensors-sirt1-and-ampk-in-lipid-induced-inflamed-adipocyte-is-regulated-by-fetuin-a
#4
Mrittika Chattopadhyay, Sandip Mukherjee, Subhendu K Chatterjee, Dipanjan Chattopadhyay, Snehasis Das, Subeer S Majumdar, Satinath Mukhopadhyay, Sutapa Mukherjee, Samir Bhattarcharya
Although several reports demonstrated that accumulation of excess lipid in adipose tissue produces defects in adipocyte which leads to the disruption of energy homeostasis causing severe metabolic problems, underlying mechanism of this event remains yet unclear. Here we demonstrate that FetuinA (FetA) plays a critical role in the impairment of two metabolic sensors, SIRT1 and AMPK, in inflamed adipocytes of high fat diet (HFD) mice. A linear increase in adipocyte hypertrophy from 10 to 16 week was in tandem with the increase in FetA and that coincided with SIRT1 cleavage and decrease in pAMPK which adversely affects PGC1α activation...
October 10, 2017: Cellular Signalling
https://www.readbyqxmd.com/read/29028772/heme-oxygenase-1-protects-the-liver-from-septic-injury-by-modulating-tlr4-mediated-mitochondrial-quality-control-in-mice
#5
Jin-Sook Park, Hyo-Sun Choi, So-Yeon Yim, Sun-Mee Lee
Mitochondrial dysfunction is involved in the pathogenesis of sepsis-induced multiple organ dysfunction syndrome (MODS). Mitochondrial quality control (QC) is characterized by self-recovering mitochondrial damage through mitochondrial biogenesis, mitophagy, and fission/fusion. Heme oxygenase (HO)-1 acts as a signaling molecule to modulate inflammation. The present study elucidated the cytoprotective mechanisms of HO-1 in sepsis, particularly focusing on toll-like receptor (TLR)4-mediated mitochondrial QC. Mice were subjected to sepsis by cecal ligation and puncture (CLP)...
October 12, 2017: Shock
https://www.readbyqxmd.com/read/29026190/growth-hormone-secretagogues-hexarelin-and-jmv2894-protect-skeletal-muscle-from-mitochondrial-damages-in-a-rat-model-of-cisplatin-induced-cachexia
#6
Giuseppe Sirago, Elena Conte, Flavio Fracasso, Antonella Cormio, Jean-Alain Fehrentz, Jean Martinez, Clara Musicco, Giulia Maria Camerino, Adriano Fonzino, Laura Rizzi, Antonio Torsello, Angela Maria Serena Lezza, Antonella Liantonio, Palmiro Cantatore, Vito Pesce
Chemotherapy can cause cachexia, which consists of weight loss associated with muscle atrophy. The exact mechanisms underlying this skeletal muscle toxicity are largely unknown and co-therapies to attenuate chemotherapy-induced side effects are lacking. By using a rat model of cisplatin-induced cachexia, we here characterized the mitochondrial homeostasis in tibialis anterior cachectic muscle and evaluated the potential beneficial effects of the growth hormone secretagogues (GHS) hexarelin and JMV2894 in this setting...
October 12, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29020013/in-utero-and-lactational-exposure-to-low-doses-of-the-pyrethroid-insecticide-cypermethrin-leads-to-neurodevelopmental-defects-in-male-mice-an-ethological-and-transcriptomic-study
#7
Anthony Laugeray, Ameziane Herzine, Olivier Perche, Olivier Richard, Céline Montecot-Dubourg, Arnaud Menuet, Séverine Mazaud-Guittot, Laurianne Lesné, Bernard Jegou, Stéphane Mortaud
Accumulating evidence suggests that developmental exposure to environmental chemicals may modify the course of brain development, ultimately leading to neuropsychiatric / neurodegenerative disorders later in life. In the present study, we assessed the impact of one of the most frequently used pesticides in both residential and agricultural applications - the synthetic pyrethroid cypermethrin (CYP) - on developmental neurotoxicity (DNT). Female mice were perinatally exposed to low doses of CYP (5 and 20 mg/kg body weight) from gestation to postnatal day 15...
2017: PloS One
https://www.readbyqxmd.com/read/28992589/epigallocatechin-3-gallate-promotes-healthy-lifespan-through-mitohormesis-during-early-to-mid-adulthood-in-caenorhabditis-elegans
#8
Li-Gui Xiong, Yi-Jun Chen, Jie-Wen Tong, Yu-Shun Gong, Jian-An Huang, Zhong-Hua Liu
The green tea polyphenol epigallocatechin-3-gallate (EGCG) is widely consumed as a dietary supplement. Its potential properties include slowing aging and extending lifespan, although how exactly this is achieved remains unclear. Here, we report that EGCG promoted healthy lifespan in Caenorhabditis elegans when administered throughout or only at early-to-mid adulthood. Specifically, EGCG extended lifespan in an inverted U-shaped dose-response manner. The life-extending mechanism was stimulated by EGCG-induced production of reactive oxygen species (ROS)...
September 29, 2017: Redox Biology
https://www.readbyqxmd.com/read/28992020/rapid-communication-dietary-selenium-improves-skeletal-muscle-mitochondrial-biogenesis-in-young-equine-athletes
#9
S H White, S Wohlgemuth, C Li, L K Warren
Exercise is known to promote mitochondrial biogenesis in skeletal muscle as well as enhance mitochondrial function and efficiency in human and rodent models. These adaptations help to decrease exercise-associated production of reactive oxygen species, which can negatively affect health and performance if antioxidant mechanisms are overwhelmed. Little is known about the adaptations of mitochondria in response to exercise training in the growing horse or if supplementation with a dietary antioxidant can improve mitochondrial function...
September 2017: Journal of Animal Science
https://www.readbyqxmd.com/read/28989247/targeting-mitochondrial-dysfunction-for-the-treatment-of-diabetic-complications-pharmacological-interventions-through-natural-products
#10
REVIEW
Aakruti Arun Kaikini, Divya Manohar Kanchan, Urvi Narayan Nerurkar, Sadhana Sathaye
Diabetes mellitus is a chronic hyperglycemic condition with deleterious effects on microcirculation, resulting in diabetic complications. Chronic hyperglycemia induces the generation of reactive oxygen species (ROS), which are the key pathological triggers in the development of diabetic complications. ROS are responsible for the activation of various pathways involved in the genesis of diabetic complications, mitochondrial dysfunction, as well as insulin resistance. The review describes normal mitochondrial physiology and abnormal alterations, which occur in response to hyperglycemia...
July 2017: Pharmacognosy Reviews
https://www.readbyqxmd.com/read/28986235/alpha-synuclein-epigenetics-mitochondria-metabolism-calcium-traffic-circadian-dysfunction-in-parkinson-s-disease-an-integrated-strategy-for-management
#11
REVIEW
Oliver T Phillipson
The motor deficits which characterise the sporadic form of Parkinson's disease arise from age-related loss of a subset of dopamine neurons in the substantia nigra. Although motor symptoms respond to dopamine replacement therapies, the underlying disease process remains. This review details some features of the progressive molecular pathology and proposes deployment of a combination of nutrients: R-lipoic acid, acetyl-l-carnitine, ubiquinol, melatonin (or receptor agonists) and vitamin D3, with the collective potential to slow progression of these features...
October 3, 2017: Ageing Research Reviews
https://www.readbyqxmd.com/read/28986187/aldose-reductase-inhibitor-fidarestat-regulates-mitochondrial-biogenesis-via-nrf2-ho-1-ampk-pathway-in-colon-cancer-cells
#12
Kirtikar Shukla, Himangshu Sonowal, Ashish Saxena, Kota V Ramana, Satish K Srivastava
Although we have shown earlier that aldose reductase (AR) inhibitors prevent colorectal cancer cell (CRC) growth in culture as well as in nude mice xenografts, the mechanism(s) is not well understood. In this study, we have investigated how AR inhibition prevents CRC growth by regulating the mitochondrial biogenesis via Nrf2/HO-1 pathway. Incubation of CRC cells such as SW-480, HT29, and HCT116 with AR inhibitor, fidarestat that non-covalently binds to the enzyme, increases the expression of Nrf2. Further, fidarestat augmented the EGF-induced expression of Nrf2 in CRC cells...
October 3, 2017: Cancer Letters
https://www.readbyqxmd.com/read/28978719/pharmacological-dual-inhibition-of-tumor-and-tumor-induced-functional-limitations-in-transgenic-model-of-breast-cancer
#13
Ruizhong Wang, Poornima Bhat-Nakshatri, Maria B Padua, Mayuri S Prasad, Manjushree Anjanappa, Max Jacobson, Courtney Finnearty, Victoria Sefcsik, Kyle McElyea, Rachael Redmond, George E Sandusky, Narsimha Penthala, Peter A Crooks, Jianguo Liu, Teresa Zimmers, Harikrishna Nakshatri
Breast cancer progression is associated with systemic effects including functional limitations and sarcopenia without the appearance of overt cachexia. Autocrine/paracrine actions of cytokines/chemokines produced by cancer cells mediate cancer progression and functional limitations. The cytokine-inducible transcription factor NF-κB could be central to this process, as it displays oncogenic functions and is integral to the Pax7:MyoD:Pgc-1β:miR-486 myogenesis axis. We tested this possibility using the MMTV-PyMT transgenic mammary tumor model and the NF-κB inhibitor dimethylaminoparthenolide (DMAPT)...
October 4, 2017: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/28971573/apigenin-ameliorates-the-obesity-induced-skeletal-muscle-atrophy-by-attenuating-mitochondrial-dysfunction-in-the-muscle-of-obese-mice
#14
Won Hee Choi, Hyo Jeong Son, Young Jin Jang, Jiyun Ahn, Chang Hwa Jung, Tae Youl Ha
SCOPE: We investigated whether apigenin protected against skeletal muscle atrophy induced by obesity. METHODS AND RESULTS: Mice were fed a high fat diet (HFD) for 9 wks to induce obesity, and then were assigned to two groups; the HFD group received a high fat diet, and the HFD+AP group received a 0.1% apigenin-containing HFD. After additional feeding of the experimental diet for 8 wks, mice in the HFD group were highly obese compared with the mice in the standard diet fed mice group...
October 2, 2017: Molecular Nutrition & Food Research
https://www.readbyqxmd.com/read/28947972/pgc1%C3%AE-induced-by-reactive-oxygen-species-contributes-to-chemoresistance-of-ovarian-cancer-cells
#15
Boyun Kim, Je Won Jung, Jaeyoung Jung, Youngjin Han, Dong Hoon Suh, Hee Seung Kim, Danny N Dhanasekaran, Yong Sang Song
Malignant cells are subjected to high levels of oxidative stress that arise from the increased production of reactive oxygen species (ROS) due to their altered metabolism. They activate antioxidant mechanisms to relieve the oxidative stress, and thereby acquire resistance to chemotherapeutic agents. In the present study, we found that PGC1α, a key molecule that both increases mitochondrial biogenesis and activates antioxidant enzymes, enhances chemoresistance in response to ROS generated by exposure of cells to ovarian sphere-forming culture conditions...
September 1, 2017: Oncotarget
https://www.readbyqxmd.com/read/28943449/inactivation-of-glycogen-synthase-kinase-3%C3%AE-gsk-3%C3%AE-enhances-skeletal-muscle-oxidative-metabolism
#16
W F Theeuwes, H R Gosker, R C J Langen, K J P Verhees, N A M Pansters, A M W J Schols, A H V Remels
BACKGROUND: Aberrant skeletal muscle mitochondrial oxidative metabolism is a debilitating feature of chronic diseases such as chronic obstructive pulmonary disease, type 2 diabetes and chronic heart failure. Evidence in non-muscle cells suggests that glycogen synthase kinase-3β (GSK-3β) represses mitochondrial biogenesis and inhibits PPAR-γ co-activator 1 (PGC-1), a master regulator of cellular oxidative metabolism. The role of GSK-3β in the regulation of skeletal muscle oxidative metabolism is unknown...
September 22, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28932194/h2s-induced-sulfhydration-biological-function-and-detection-methodology
#17
REVIEW
Da Zhang, Junbao Du, Chaoshu Tang, Yaqian Huang, Hongfang Jin
At appropriate concentrations, hydrogen sulfide, a well-known gasotransmitter, plays important roles in both physiology and pathophysiology. Increasing evidence suggests that modifying thiol groups of specific cysteines in target proteins via sulfhydration or persulfidation is one of the important mechanisms responsible for the biological functions of hydrogen sulfide. A variety of key proteins of different cellular pathways in mammals have been reported to be sulfhydrated by hydrogen sulfide to participate and regulate the processes of cell survival/death, cell differentiation, cell proliferation/hypertrophy, cellular metabolism, mitochondrial bioenergetics/biogenesis, endoplasmic reticulum stress, vasorelaxtion, inflammation, oxidative stress, etc...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28920922/g%C3%AE-13-ablation-reprograms-myofibers-to-oxidative-phenotype-and-enhances-whole-body-metabolism
#18
Ja Hyun Koo, Tae Hyun Kim, Shi-Young Park, Min Sung Joo, Chang Yeob Han, Cheol Soo Choi, Sang Geon Kim
Skeletal muscle is a key organ in energy homeostasis owing to its high requirement for nutrients. Heterotrimeric G proteins converge signals from cell-surface receptors to potentiate or blunt responses against environmental changes. Here, we show that muscle-specific ablation of Gα13 in mice promotes reprogramming of myofibers to the oxidative type, with resultant increases in mitochondrial biogenesis and cellular respiration. Mechanistically, Gα13 and its downstream effector RhoA suppressed nuclear factor of activated T cells 1 (NFATc1), a chief regulator of myofiber conversion, by increasing Rho-associated kinase 2-mediated (Rock2-mediated) phosphorylation at Ser243...
October 2, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28918598/triacsin-c-reduces-lipid-droplet-formation-and-induces-mitochondrial-biogenesis-in-primary-rat-hepatocytes
#19
Carlos R P Dechandt, Felippe H Zuccolotto-Dos-Reis, Bruno G Teodoro, Anna Maria A P Fernandes, Marcos N Eberlin, Isis C Kettelhut, Carlos Curti, Luciane C Alberici
Intracellular long-chain acyl-CoA synthetases (ACSL) activate fatty acids to produce acyl-CoA, which undergoes β-oxidation and participates in the synthesis of esterified lipids such as triacylglycerol (TAG). Imbalances in these metabolic routes are closely associated with the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Triacsin C is one of the few compounds that inhibit TAG accumulation into lipid droplets (LD) by suppressing ACSL activity. Here we report that treatment of primary rat hepatocytes with triacsin C at concentrations lower than the IC50 (4...
September 16, 2017: Journal of Bioenergetics and Biomembranes
https://www.readbyqxmd.com/read/28916822/ampk-phosphorylation-of-ulk1-is-required-for-targeting-of-mitochondria-to-lysosomes-in-exercise-induced-mitophagy
#20
Rhianna C Laker, Joshua C Drake, Rebecca J Wilson, Vitor A Lira, Bevan M Lewellen, Karen A Ryall, Carleigh C Fisher, Mei Zhang, Jeffrey J Saucerman, Laurie J Goodyear, Mondira Kundu, Zhen Yan
Mitochondrial health is critical for skeletal muscle function and is improved by exercise training through both mitochondrial biogenesis and removal of damaged/dysfunctional mitochondria via mitophagy. The mechanisms underlying exercise-induced mitophagy have not been fully elucidated. Here, we show that acute treadmill running in mice causes mitochondrial oxidative stress at 3-12 h and mitophagy at 6 h post-exercise in skeletal muscle. These changes were monitored using a novel fluorescent reporter gene, pMitoTimer, that allows assessment of mitochondrial oxidative stress and mitophagy in vivo, and were preceded by increased phosphorylation of AMP activated protein kinase (Ampk) at tyrosine 172 and of unc-51 like autophagy activating kinase 1 (Ulk1) at serine 555...
September 15, 2017: Nature Communications
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