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https://www.readbyqxmd.com/read/28213158/pink1-parkin-mitophagy-and-neurodegeneration-what-do-we-really-know-in-vivo
#1
REVIEW
Alexander J Whitworth, Leo J Pallanck
Mitochondria are essential organelles that provide cellular energy and buffer cytoplasmic calcium. At the same time they produce damaging reactive oxygen species and sequester pro-apoptotic factors. Hence, eukaryotes have evolved exquisite homeostatic processes that maintain mitochondrial integrity, or ultimately remove damaged organelles. This subject has garnered intense interest recently following the discovery that two Parkinson's disease genes, PINK1 and parkin, regulate mitochondrial degradation (mitophagy)...
February 14, 2017: Current Opinion in Genetics & Development
https://www.readbyqxmd.com/read/28213011/calorie-restriction-promotes-cardiolipin-biosynthesis-and-distribution-between-mitochondrial-membranes
#2
Luis Alberto Luévano-Martínez, Maria Fernanda Forni, Julia Peloggia, Ii-Sei Watanabe, Alicia J Kowaltowski
Calorie restriction (CR) has been amply demonstrated to modify mitochondrial function. However, little is known regarding the effects of this dietary regimen on mitochondrial membranes. We isolated phospholipids from rat liver mitochondria from animals on CR or ad libitum diets and found that mitochondria from ad libitum animals present an increased content of lipoperoxides and the content of cardiolipin. Cardiolipin is the main anionic phospholipid present in mitochondrial membranes, and plays a key role in mitochondrial function, signaling and stress response...
February 14, 2017: Mechanisms of Ageing and Development
https://www.readbyqxmd.com/read/28212735/elimination-of-the-unnecessary-intra-and-extracellular-signaling-by-anionic-phospholipids
#3
REVIEW
Valerian E Kagan, Hülya Bayır, Yulia Y Tyurina, Sergey B Bolevich, John J Maguire, Bengt Fadeel, Krishnakumar Balasubramanian
High fidelity of biological systems is frequently achieved by duplication of the essential intracellular machineries or, removal of the entire cell, which becomes unnecessary or even harmful in altered physiological environments. Carefully controlled removal of these cells, without damaging normal cells, requires precise signaling, and is critical to maintaining homeostasis. This review describes how two anionic phospholipids - phosphatidylserine (PS) and cardiolipin (CL) - residing in distinct compartments of the cell, signal removal of "the unnecessary" using several uniform principles...
January 15, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28212727/mitophagy-link-to-cancer-development-and-therapy
#4
REVIEW
Andrey V Kulikov, Ekaterina A Luchkina, Vladimir Gogvadze, Boris Zhivotovsky
Mitophagy, the selective degradation of mitochondria via the autophagic pathway, is a vital mechanism of mitochondrial quality control in cells. Mitophagy is responsible for the removal of malfunctioning or damaged mitochondria, which is essential for normal cellular physiology and tissue development. Pathways involved in the regulation of mitophagy, tumorigenesis, and cell death are overlapping in many cases and may be triggered by common upstream signals, which converge at the mitochondria. The failure to properly modulate mitochondrial turnover in response to oncogenic stresses can either stimulate or suppress tumorigenesis...
January 15, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28211814/are-major-dementias-triggered-by-poor-blood-flow-to-the-brain-theoretical-considerations
#5
Jack C de la Torre
There is growing evidence that chronic brain hypoperfusion plays a central role in the development of Alzheimer's disease (AD) long before dyscognitive symptoms or amyloid-β accumulation in the brain appear. This commentary proposes that dementia with Lewy bodies (DLB), frontotemporal dementia (FTD), and Creutzfeldt-Jakob disease (CJD) may also develop from chronic brain hypoperfusion following a similar but not identical neurometabolic breakdown as AD. The argument to support this conclusion is that chronic brain hypoperfusion, which is found at the early stages of the three dementias reviewed here, will reduce oxygen delivery and lower oxidative phosphorylation promoting a steady decline in the synthesis of the cell energy fuel adenosine triphosphate (ATP)...
February 15, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28210805/transcutaneous-carbon-dioxide-application-accelerates-muscle-injury-repair-in-rat-models
#6
Shiho Akahane, Yoshitada Sakai, Takeshi Ueha, Hanako Nishimoto, Miho Inoue, Takahiro Niikura, Ryosuke Kuroda
PURPOSE: Skeletal muscle injuries are commonly observed in sports and traumatology medicine. Previously, we demonstrated that transcutaneous application of carbon dioxide (CO2) to lower limbs increased the number of muscle mitochondria and promoted muscle endurance. Therefore, we aimed to investigate whether transcutaneous CO2 application could enhance recovery from muscle injury. METHODS: Tibialis anterior muscle damage was induced in 27 Sprague Dawley rats via intramuscular injection of bupivacaine...
February 16, 2017: International Orthopaedics
https://www.readbyqxmd.com/read/28208064/mitochondrial-genes-are-altered-in-blood-early-in-alzheimer-s-disease
#7
Katie Lunnon, Aoife Keohane, Ruth Pidsley, Stephen Newhouse, Joanna Riddoch-Contreras, Elisabeth B Thubron, Matthew Devall, Hikka Soininen, Iwona Kłoszewska, Patrizia Mecocci, Magda Tsolaki, Bruno Vellas, Leonard Schalkwyk, Richard Dobson, Afshan N Malik, John Powell, Simon Lovestone, Angela Hodges
Although mitochondrial dysfunction is a consistent feature of Alzheimer's disease in the brain and blood, the molecular mechanisms behind these phenomena are unknown. Here we have replicated our previous findings demonstrating reduced expression of nuclear-encoded oxidative phosphorylation (OXPHOS) subunits and subunits required for the translation of mitochondrial-encoded OXPHOS genes in blood from people with Alzheimer's disease and mild cognitive impairment. Interestingly this was accompanied by increased expression of some mitochondrial-encoded OXPHOS genes, namely those residing closest to the transcription start site of the polycistronic heavy chain mitochondrial transcript (MT-ND1, MT-ND2, MT-ATP6, MT-CO1, MT-CO2, MT-C03) and MT-ND6 transcribed from the light chain...
January 7, 2017: Neurobiology of Aging
https://www.readbyqxmd.com/read/28206987/id2-promotes-survival-of-glioblastoma-cells-during-metabolic-stress-by-regulating-mitochondrial-function
#8
Zhonghua Zhang, Gilbert J Rahme, Pranam D Chatterjee, Matthew C Havrda, Mark A Israel
Tumor cells proliferate in cellular environments characterized by a lack of optimal tissue organization resulting oftentimes in compromised cellular metabolism affecting nutrition, respiration, and energetics. The response of tumor cells to adverse environmental conditions is a key feature affecting their pathogenicity. We found that inhibitor of DNA binding 2 (ID2) expression levels significantly correlate with the ability of glioblastoma (GBM)-derived cell lines to survive glucose deprivation. ID2 suppressed mitochondrial oxidative respiration and mitochondrial ATP production by regulating the function of mitochondrial electron transport chain (mETC) complexes, resulting in reduced superoxide and reactive oxygen species (ROS) production from mitochondria...
February 16, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28203548/doxycycline-induces-mitophagy-and-suppresses-production-of-interferon-%C3%AE-in-ipec-j2-cells
#9
Yang Xing, Zhu Liqi, Lin Jian, Yu Qinghua, Yang Qian
Previous reports have demonstrated that the second-generation tetracycline derivative doxycycline (DOX) interrupts mitochondrial proteostasis and physiology, inhibits proliferation of many cell types, and induces apoptosis. However, the effects of DOX, which is widely used in porcine husbandry by feed, on the porcine intestinal epithelium are unclear. In this study, we demonstrated that DOX damaged mitochondrial morphology and induced the co-localization of mitochondria with autophagosomes, suggesting that DOX induces mitophagy in IPEC-J2 cells...
2017: Frontiers in Cellular and Infection Microbiology
https://www.readbyqxmd.com/read/28202400/protective-role-of-mitochondrial-peroxiredoxin-iii-against-uvb-induced-apoptosis-of-epidermal-keratinocytes
#10
Jin Young Baek, Sujin Park, Jiyoung Park, Ji Yong Jang, Su Bin Wang, Sin Ri Kim, Hyun Ae Woo, Kyung Min Lim, Tong-Shin Chang
Ultraviolet B (UVB) light induces generation of reactive oxygen species (ROS), ultimately leading to skin cell damage. Mitochondria are a major source of ROS in UVB-irradiated skin cells, with increased levels of mitochondrial ROS having been implicated in keratinocyte apoptosis. Peroxiredoxin III (PrxIII) is the most abundant and potent H2O2-removing enzyme in the mitochondria of most cell types. Here, the protective role of PrxIII against UVB-induced apoptosis of epidermal keratinocytes was investigated. Mitochondrial H2O2 levels were differentiated from other types of ROS using mitochondria-specific fluorescent H2O2 indicators...
February 12, 2017: Journal of Investigative Dermatology
https://www.readbyqxmd.com/read/28202127/-role-of-mitophagy-in-neonatal-rats-with-hypoxic-ischemic-brain-damage
#11
Ming-Xi Li, Yi Qu, De-Zhi Mu
OBJECTIVE: To investigate mitophagy in an animal model of hypoxic-ischemic brain damage (HIBD) and its role in HIBD. METHODS: A total of 120 neonatal Sprague-Dawley rats aged 7 days were divided into three groups: sham-operation, HIBD, and autophagy inhibitor intervention (3MA group). The rats in the HIBD group were treated with right common carotid artery ligation and then put in a hypoxic chamber (8% oxygen and 92% nitrogen) for 2.5 hours. Those in the 3MA group were given ligation and hypoxic treatment at 30 minutes after intraperitoneal injection of 2 μL 3MA...
February 2017: Zhongguo Dang Dai Er Ke za Zhi, Chinese Journal of Contemporary Pediatrics
https://www.readbyqxmd.com/read/28199200/mitochondrial-dna-mitochondrial-dysfunction-and-cardiac-manifestations
#12
Sung Ryul Lee, Nari Kim, Yeun Hee Noh, Zhelong Xu, Kyung Soo Ko, Byoung Doo Rhee, Jin Han
Mitochondria, are the powerhouses of cells, have their own DNA (mtDNA), regulate the transport of metabolites and ions, and impact cell physiology, survival, and death. Mitochondrial dysfunction, including impaired oxidative phosphorylation, preferentially affects heart function due to an imbalance of energy supply and demand. Recently, mitochondrial mutations and associated mitochondrial dysfunction were suggested as a causal factor of cardiac manifestations. Oxidative stress largely influences mtDNA stability due to oxidative modifications of mtDNA...
March 1, 2017: Frontiers in Bioscience (Landmark Edition)
https://www.readbyqxmd.com/read/28195557/biogenetic-and-morphofunctional-heterogeneity-of-mitochondria-the-case-of-synaptic-mitochondria
#13
Sergei V Fedorovich, Tatyana V Waseem, Ludmila V Puchkova
The mitochondria of different cells are different in their morphological and biochemical properties. These organelles generate free radicals during activity, leading inevitably to mitochondrial DNA damage. It is not clear how this problem is addressed in long-lived cells, such as neurons. We propose the hypothesis that mitochondria within the same cell also differ in lifespan and ability to divide. According to our suggestion, cells have a pool of 'stem' mitochondria with low metabolic activity and a pool of 'differentiated' mitochondria with significantly shorter lifespans and high metabolic activity...
February 14, 2017: Reviews in the Neurosciences
https://www.readbyqxmd.com/read/28194437/mitochondrial-quality-control-dysregulation-in-conditional-ho-1-mice
#14
Hagir B Suliman, Jeffrey E Keenan, Claude A Piantadosi
The heme oxygenase-1 (Hmox1; HO-1) pathway was tested for defense of mitochondrial quality control in cardiomyocyte-specific Hmox1 KO mice (HO-1[CM](-/-)) exposed to oxidative stress (100% O2). After 48 hours of exposure, these mice showed persistent cardiac inflammation and oxidative tissue damage that caused sarcomeric disruption, cardiomyocyte death, left ventricular dysfunction, and cardiomyopathy, while control hearts showed minimal damage. After hyperoxia, HO-1(CM)(-/-) hearts showed suppression of the Pgc-1α/nuclear respiratory factor-1 (NRF-1) axis, swelling, low electron density mitochondria by electron microscopy (EM), increased cell death, and extensive collagen deposition...
February 9, 2017: JCI Insight
https://www.readbyqxmd.com/read/28193566/in-vitro-evaluation-of-ruthenium-complexes-for-photodynamic-therapy
#15
Wenna Li, Qiang Xie, Linglin Lai, Zhentao Mo, Xiaofang Peng, Ennian Leng, Dandan Zhang, Hongxia Sun, Yiqi Li, Wenjie Mei, Shuying Gao
BACKGROUND: Photodynamic therapy (PDT) is a promising new anti-tumor treatment strategy. Photosensitizer is one of the most important components of PDT. In this work, the anticancer activities of PDTs mediated by six new ruthenium porphyrin complexes were screened. The mechanisms of the most efficacious candidate were investigated. METHODS: Photocytotoxicity of the six porphyrins was tested. The most promising complex, Rup-03, was further investigated using Geimsa staining, which indirectly detects reactive oxygen species (ROS) and subcellular localization...
February 10, 2017: Photodiagnosis and Photodynamic Therapy
https://www.readbyqxmd.com/read/28192157/apaf-1-regulation-and-function-in-cell-death
#16
REVIEW
Raheleh Shakeri, Asma Kheirollahi, Jamshid Davoodi
Apoptosis, a form of programmed cell death, is responsible for eliminating damaged or unnecessary cells in multicellular organisms. Various types of intracellular stress trigger apoptosis by induction of cytochrome c release from mitochondria into the cytosol. Apoptotic protease activating factor-1 (Apaf-1) is a key molecule in the intrinsic or mitochondrial pathway of apoptosis, which oligomerizes in response to cytochrome c release and forms a large complex known as apoptosome. Procaspase-9, an initiator caspase in the mitochondrial pathway, is recruited and activated by the apoptosome leading to downstream caspase-3 processing...
February 9, 2017: Biochimie
https://www.readbyqxmd.com/read/28191272/mitochondrial-ferritin-deletion-exacerbates-%C3%AE-amyloid-induced-neurotoxicity-in-mice
#17
Peina Wang, Qiong Wu, Wenyue Wu, Haiyan Li, Yuetong Guo, Peng Yu, Guofen Gao, Zhenhua Shi, Baolu Zhao, Yan-Zhong Chang
Mitochondrial ferritin (FtMt) is a mitochondrial iron storage protein which protects mitochondria from iron-induced oxidative damage. Our previous studies indicate that FtMt attenuates β-amyloid- and 6-hydroxydopamine-induced neurotoxicity in SH-SY5Y cells. To explore the protective effects of FtMt on β-amyloid-induced memory impairment and neuronal apoptosis and the mechanisms involved, 10-month-old wild-type and Ftmt knockout mice were infused intracerebroventricularly (ICV) with Aβ25-35 to establish an Alzheimer's disease model...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28190529/mitophagy-and-alzheimer-s-disease-cellular-and-molecular-mechanisms
#18
REVIEW
Jesse S Kerr, Bryan A Adriaanse, Nigel H Greig, Mark P Mattson, M Zameel Cader, Vilhelm A Bohr, Evandro F Fang
Neurons affected in Alzheimer's disease (AD) experience mitochondrial dysfunction and a bioenergetic deficit that occurs early and promotes the disease-defining amyloid beta peptide (Aβ) and Tau pathologies. Emerging findings suggest that the autophagy/lysosome pathway that removes damaged mitochondria (mitophagy) is also compromised in AD, resulting in the accumulation of dysfunctional mitochondria. Results in animal and cellular models of AD and in patients with sporadic late-onset AD suggest that impaired mitophagy contributes to synaptic dysfunction and cognitive deficits by triggering Aβ and Tau accumulation through increases in oxidative damage and cellular energy deficits; these, in turn, impair mitophagy...
February 9, 2017: Trends in Neurosciences
https://www.readbyqxmd.com/read/28188904/exposure-to-cadmium-during-in-vitro-maturation-at-environmental-nanomolar-levels-impairs-oocyte-fertilization-through-oxidative-damage-a-large-animal-model-study
#19
N A Martino, G Marzano, M Mangiacotti, O Miedico, A M Sardanelli, A Gnoni, G M Lacalandra, A E Chiaravalle, E Ciani, L Bogliolo, F Minervini, F Pizzi, M E Dell'Aquila
Cadmium is a highly toxic heavy metal with negative effects on oocyte fertilization. The aim of this study was to analyse whether cadmium-induced impairment of fertilization is caused by mitochondria dysfunction and oxidative stress in the cumulus-oocyte complex (COC). Preliminarily, 19 trace element levels were measured in ovaries from juvenile and adult ewes and age-related cadmium ovarian bioaccumulation at nanomolar concentrations was found. COCs from juvenile and adult ewes, exposed during in vitro maturation to 1nM or 100nM CdCl2, and subjected to in vitro fertilization showed significantly lower fertilization rates in exposed COCs compared with controls...
February 7, 2017: Reproductive Toxicology
https://www.readbyqxmd.com/read/28185435/evidence-that-a-mitochondrial-death-spiral-underlies-antagonistic-pleiotropy
#20
REVIEW
Michael Stern
The antagonistic pleiotropy (AP) theory posits that aging occurs because alleles that are detrimental in older organisms are beneficial to growth early in life and thus are maintained in populations. Although genes of the insulin signaling pathway likely participate in AP, the insulin-regulated cellular correlates of AP have not been identified. The mitochondrial quality control process called mitochondrial autophagy (mitophagy), which is inhibited by insulin signaling, might represent a cellular correlate of AP...
February 9, 2017: Aging Cell
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