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https://www.readbyqxmd.com/read/29028772/heme-oxygenase-1-protects-the-liver-from-septic-injury-by-modulating-tlr4-mediated-mitochondrial-quality-control-in-mice
#1
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
#2
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/29021295/mitochondrial-cardiomyopathy-caused-by-elevated-reactive-oxygen-species-and-impaired-cardiomyocyte-proliferation
#3
Donghui Zhang, Yifei Li, Danielle A Heims-Waldron, Vassilios J Bezzerides, Silvia Guatimosim, Yuxuan Guo, Fei Gu, Pingzhu Zhou, Zhiqiang Lin, Qing Ma, Jianming Liu, Da-Zhi Wang, William T Pu
Rationale: Although mitochondrial diseases often cause abnormal myocardial development, the mechanisms by which mitochondria influence heart growth and function are poorly understood. Objective: To investigate these disease mechanisms, we studied a genetic model of mitochondrial dysfunction caused by inactivation of Tfam (Transcription Factor A, Mitochondrial), a nuclear-encoded gene that is essential for mitochondrial gene transcription and mitochondrial DNA replication. Methods and Results:Tfam inactivation by Nkx2...
October 11, 2017: Circulation Research
https://www.readbyqxmd.com/read/28986187/aldose-reductase-inhibitor-fidarestat-regulates-mitochondrial-biogenesis-via-nrf2-ho-1-ampk-pathway-in-colon-cancer-cells
#4
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/28975969/research-on-biogenesis-of-mitochondria-in-astrocytes-in-sepsis-associated-encephalopathy-models
#5
Y-Z Zhao, Z-Y Gao, L-Q Ma, Y-Y Zhuang, F-L Guan
OBJECTIVE: To study the structural and functional changes in mitochondria in astrocytes of the cerebral cortex of the rats in the simulated sepsis environment in vitro and the relationship between these changes and the biogenesis of mitochondria in astrocytes by establishing models of sepsis astrocytes. MATERIALS AND METHODS: The structural and functional changes in mitochondria in astrocytes of the cerebral cortex of the rats were evaluated. The ultra structural changes in the mitochondria, astrocytes, and ultrathin sections, were observed with a transmission electron microscope...
October 2017: European Review for Medical and Pharmacological Sciences
https://www.readbyqxmd.com/read/28973648/the-nad-dependent-deacetylase-sirt2-attenuates-oxidative-stress-and-mitochondrial-dysfunction-and-improves-insulin-sensitivity-in-hepatocytes
#6
Vera Lemos, Rita M Oliveira, Luana Naia, Eva Szego, Elisabete Ramos, Sónia Pinho, Fernando Magro, Cláudia Cavadas, A Cristina Rego, Vítor Costa, Tiago F Outeiro, Pedro Gomes
Insulin resistance is a major predictor of the development of metabolic disorders. Sirtuins (SIRTs) have emerged as potential targets that can be manipulated to counteract age-related diseases, including type 2 diabetes. SIRT2 has been recently shown to exert important metabolic effects, but whether SIRT2 regulates insulin sensitivity in hepatocytes is currently unknown. The aim of this study is to investigate this possibility and to elucidate underlying molecular mechanisms. Here we show that SIRT2 is downregulated in insulin-resistant hepatocytes and livers and this was accompanied by increased generation of reactive oxygen species (ROS), activation of stress-sensitive ERK1/2 kinase, and mitochondrial dysfunction...
July 26, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28969026/increasing-ucp2-expression-and-decreasing-nox1-4-expression-maintain-chondrocyte-phenotype-by-reducing-reactive-oxygen-species-production
#7
Yansong Miao, Yuefu Dong, Ping Huang, Xiang Zhao, Zhenyu Huang, Jufang Yao, He Li, Qingrong Xu
The aim of this study is to demonstrate that improving the mitochondrial function can inhibite the loss of chondrocyte phenotype by regulating the expression of uncoupling protein 2(UCP2) and NADPH oxidase1/4(NOX1/4) to reduce the production of reactive oxygen species(ROS). The effects of mitochondrial biogenesis "master regular" peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α), mitochondrial transcriptional factor A (TFAM), UCP2, and NOX1/4 on chondrocyte phenotype was examined. It was found that when the chondrocyte phenotype was lost, PGC-1α, UCP2, and TFAM expression decreased, while NOX1/4 expression increased...
September 8, 2017: Oncotarget
https://www.readbyqxmd.com/read/28964868/the-neuroprotective-role-of-rosiglitazone-in-advanced-glycation-end-product-treated-human-neural-stem-cells-is-ppargamma-dependent
#8
Ming-Chang Chiang, Yi-Chuan Cheng, Christopher J Nicol, Chien-Hung Lin
Hyperglycemia is accompanied by an accelerated formation rate of advanced glycation end products (AGEs), which is associated with the pathogenesis of diabetic neuronal deficits. Peroxisome proliferator-activated receptor gamma (PPARγ) belongs to a family of ligand-activated nuclear receptors and its ligands are known to control many physiological, pathological and inflammatory pathways. Weinvestigated the hypothesis that the PPARγ agonist (rosiglitazone) would abrogate AGEs-mediated neurotoxic effects on human neural stem cells (hNSCs), by whichAGEs may play a role in diabetic-related neuronal impairment...
September 28, 2017: International Journal of Biochemistry & Cell Biology
https://www.readbyqxmd.com/read/28962857/mitochondrial-cardiomyopathies-feature-increased-uptake-and-diminished-efflux-of-mitochondrial-calcium
#9
Salah Sommakia, Patrick R Houlihan, Sadiki S Deane, Judith A Simcox, Natalia S Torres, Mi-Young Jeong, Dennis R Winge, Claudio J Villanueva, Dipayan Chaudhuri
Calcium (Ca(2+)) influx into the mitochondrial matrix stimulates ATP synthesis. Here, we investigate whether mitochondrial Ca(2+) transport pathways are altered in the setting of deficient mitochondrial energy synthesis, as increased matrix Ca(2+) may provide a stimulatory boost. We focused on mitochondrial cardiomyopathies, which feature such dysfunction of oxidative phosphorylation. We study a mouse model where the main transcription factor for mitochondrial DNA (transcription factor A, mitochondrial, Tfam) has been disrupted selectively in cardiomyocytes...
September 28, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28958595/the-mtdna-replication-related-genes-tfam-and-polg-are-associated-with-leprosy-in-han-chinese-from-southwest-china
#10
Dong Wang, Guo-Dong Li, Yu Fan, Deng-Feng Zhang, Rui Bi, Xiu-Feng Yu, Heng Long, Yu-Ye Li, Yong-Gang Yao
BACKGROUND: The pathogen Mycobacterium leprae of leprosy is heavily dependent on the host energy metabolites and nutritional products for survival. Previously we and others have identified associations of several mitochondrion-related genes and mitochondrial DNA (mtDNA) copy number alterations with leprosy and/or its subtype. We hypothesized that genetic variants of mtDNA replication-related genes would affect leprosy. OBJECTIVE: We aimed to identify genetic associations between the mtDNA replication-related genes TFAM, POLG and leprosy...
September 14, 2017: Journal of Dermatological Science
https://www.readbyqxmd.com/read/28934520/damage-of-inner-ear-sensory-hair-cells-via-mitochondrial-loss-in-a-murine-model-of-sleep-apnea-with-chronic-intermittent-hypoxia
#11
Young Joon Seo, Hyun Mi Ju, Sun Hee Lee, Sang Hyun Kwak, Min Jung Kang, Joo-Heon Yoon, Chang-Hoon Kim, Hyung-Ju Cho
Study Objectives: Investigating the exact pathophysiology of obstructive sleep apnea syndrome (OSAS)-induced hearing loss is critical. We sought to verify the hypothesis that a correlation exists between mitochondrial dysfunction in inner ear hair cells and the auditory dysfunction induced by chronic intermittent hypoxia (CIH) in a murine model of sleep apnea. Methods: C57BL/6J adult male mice were randomized to 4 weeks of CIH (n = 12) or normoxia (Sham) (n = 12)...
September 1, 2017: Sleep
https://www.readbyqxmd.com/read/28915557/loss-of-p16-ink4a-stimulates-aberrant-mitochondrial-biogenesis-through-a-cdk4-rb-independent-pathway
#12
Ethika Tyagi, Bin Liu, Chelsea Li, Tong Liu, Jared Rutter, Douglas Grossman
The tumor suppressor p16INK4A (p16) inhibits cell cycle progression through the CDK4/Rb pathway. We have previously shown that p16 regulates cellular oxidative stress, independent of its role in cell cycle control. We investigated whether loss of p16 had a direct impact on the mitochondria. We found that p16-null primary mouse fibroblasts (PMFs) displayed increased mitochondrial mass and expression of mitochondrial respiratory subunit proteins compared to wild-type (WT) PMFs. These findings in p16-null PMFs were associated with increased expression of the mitochondrial biogenesis transcription factors PRC and TFAM...
August 22, 2017: Oncotarget
https://www.readbyqxmd.com/read/28906435/mitochondrial-biogenesis-in-response-to-chromium-vi-toxicity-in-human-liver-cells
#13
Xiali Zhong, Rita de Cássia da Silveira E Sá, Caigao Zhong
Hexavalent chromium (Cr(VI)) is a ubiquitous environmental pollutant, which poses a threat to human public health. Recent studies have shown that mitochondrial biogenesis can be activated by inflammatory and oxidative stress. However, whether mitochondrial biogenesis is involved in Cr(VI)-induced hepatotoxicity is unclear. Here, we demonstrated the induction of inflammatory response and oxidative stress, as indicated by upregulation of inflammatory factors and reactive oxygen species (ROS). Subsequently, we demonstrated that mitochondrial biogenesis, comprising the mitochondrial DNA copy number and mitochondrial mass, was significantly increased in HepG2 cells exposed to low concentrations of Cr(VI)...
September 14, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28902841/cgas-senses-long-and-hmgb-tfam-bound-u-turn-dna-by-forming-protein-dna-ladders
#14
Liudmila Andreeva, Björn Hiller, Dirk Kostrewa, Charlotte Lässig, Carina C de Oliveira Mann, David Jan Drexler, Andreas Maiser, Moritz Gaidt, Heinrich Leonhardt, Veit Hornung, Karl-Peter Hopfner
Cytosolic DNA arising from intracellular pathogens triggers a powerful innate immune response. It is sensed by cyclic GMP-AMP synthase (cGAS), which elicits the production of type I interferons by generating the second messenger 2'3'-cyclic-GMP-AMP (cGAMP). Endogenous nuclear or mitochondrial DNA can also be sensed by cGAS under certain conditions, resulting in sterile inflammation. The cGAS dimer binds two DNA ligands shorter than 20 base pairs side-by-side, but 20-base-pair DNA fails to activate cGAS in vivo and is a poor activator in vitro...
September 21, 2017: Nature
https://www.readbyqxmd.com/read/28900194/live-imaging-reveals-the-dynamics-and-regulation-of-mitochondrial-nucleoids-during-the-cell-cycle-in-fucci2-hela-cells
#15
Taeko Sasaki, Yoshikatsu Sato, Tetsuya Higashiyama, Narie Sasaki
Mitochondrial DNA (mtDNA) is organized in nucleoprotein complexes called mitochondrial nucleoids (mt-nucleoids), which are critical units of mtDNA replication and transmission. In humans, several hundreds of mt-nucleoids exist in a cell. However, how numerous mt-nucleoids are maintained during the cell cycle remains elusive, because cell cycle synchronization procedures affect mtDNA replication. Here, we analyzed regulation of the maintenance of mt-nucleoids in the cell cycle, using a fluorescent cell cycle indicator, Fucci2...
September 12, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28884876/intranasal-insulin-treatment-restores-cognitive-deficits-and-insulin-signaling-impairment-induced-by-repeated-methamphetamine-exposure
#16
Elmira Beirami, Shahrbanoo Oryan, Seyedeh Masoumeh Seyedhoseini Tamijani, Abolhassan Ahmadiani, Leila Dargahi
Long-term use of methamphetamine (MA) causes a broad range of cognitive deficits. Recently, it has been reported insulin signaling and mitochondrial biogenesis are involved in cognitive processes. This study aimed to examine whether MA induces cognitive deficits concomitant with insulin signaling impairment and mitochondrial dysfunctions and also intranasal (IN) insulin treatment can reverse cognitive deficits caused by MA. Rats were repeatedly treated with increasing doses of MA (1-10 mg/kg) twice a day for 10 days, and their cognitive functions were assessed using Y-maze, novel object recognition and passive avoidance tasks...
September 8, 2017: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/28883902/sirt1-activation-by-resveratrol-alleviates-cardiac-dysfunction-via-mitochondrial-regulation-in-diabetic-cardiomyopathy-mice
#17
Sai Ma, Jing Feng, Ran Zhang, Jiangwei Chen, Dong Han, Xiang Li, Bo Yang, Xiujuan Li, Miaomiao Fan, Congye Li, Zuhong Tian, Yabin Wang, Feng Cao
BACKGROUND: Diabetic cardiomyopathy (DCM) is a major threat for diabetic patients. Silent information regulator 1 (SIRT1) has a regulatory effect on mitochondrial dynamics, which is associated with DCM pathological changes. Our study aims to investigate whether resveratrol, a SRIT1 activator, could exert a protective effect against DCM. METHODS AND RESULTS: Cardiac-specific SIRT1 knockout (SIRT1(KO)) mice were generated using Cre-loxP system. SIRT1(KO) mice displayed symptoms of DCM, including cardiac hypertrophy and dysfunction, insulin resistance, and abnormal glucose metabolism...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28864016/effects-of-maternal-diabetes-and-fetal-sex-on-human-placenta-mitochondrial-biogenesis
#18
Shaoning Jiang, April M Teague, Jeanie B Tryggestad, Christopher E Aston, Timothy Lyons, Steven D Chernausek
Abnormal placental function in maternal diabetes affects fetal health and can predispose offspring to metabolic diseases in later life. There are fetal sex-specific differences in placenta structure and gene expression, which may affect placental responses to maternal diabetes. The present study examined the effects of maternal diabetes on indices of mitochondrial biogenesis in placentae from male and female offspring. Mitochondrial DNA (mtDNA) copy number and expression of key regulators of mitochondrial biogenesis were assessed in placentae from 19 diabetic and 23 non-diabetic women...
September 2017: Placenta
https://www.readbyqxmd.com/read/28841355/topological-requirements-of-the-mitochondrial-heavy-strand-promoters
#19
Ornella Zollo, Neal Sondheimer
In vitro studies of mitochondrial transcription often use linear templates that fail to replicate key features of transcription on a circular genome. We developed a plasmid-based system for the analysis of heavy-strand promoters that recapitulates key features of native mtDNA to study topological and protein requirements of promoter activation. The heavy-strand promoters (HSP1 and HSP2) are simultaneously active on a circular template. HSP2 requires supercoiling for maximal activation. Increasing TFAM concentrations suppress HSP2 at levels that result in HSP1 stimulation...
August 25, 2017: Transcription
https://www.readbyqxmd.com/read/28831286/standardized-kaempferia-parviflora-extract-inhibits-intrinsic-aging-process-in-human-dermal-fibroblasts-and-hairless-mice-by-inhibiting-cellular-senescence-and-mitochondrial-dysfunction
#20
Ji-Eun Park, Seon Wook Woo, Mi-Bo Kim, Changhee Kim, Jae-Kwan Hwang
Intrinsic skin aging is a complex biological phenomenon mainly caused by cellular senescence and mitochondrial dysfunction. This study evaluated the inhibitory effect of Kaempferia parviflora Wall ex. Baker ethanol extract (KPE) on H2O2-stimulated cellular senescence and mitochondrial dysfunction both in vitro and in vivo. KPE significantly increased cell growth and suppressed senescence-associated β-galactosidase activation. KPE inhibited the expression of cell-cycle inhibitors (p53, p21, p16, and pRb) and stimulated the expression of cell-cycle activators (E2F1 and E2F2)...
2017: Evidence-based Complementary and Alternative Medicine: ECAM
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