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mitochondrial copy number

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https://www.readbyqxmd.com/read/29050365/mitochondrial-genome-variation-and-prostate-cancer-a-review-of-the-mutational-landscape-and-application-to-clinical-management
#1
REVIEW
Anton M F Kalsbeek, Eva K F Chan, Niall M Corcoran, Christopher M Hovens, Vanessa M Hayes
Prostate cancer is a genetic disease. While next generation sequencing has allowed for the emergence of molecular taxonomy, classification is restricted to the nuclear genome. Mutations within the maternally inherited mitochondrial genome are known to impact cancer pathogenesis, as a result of disturbances in energy metabolism and apoptosis. With a higher mutation rate, limited repair and increased copy number compared to the nuclear genome, the clinical relevance of mitochondrial DNA (mtDNA) variation requires deeper exploration...
September 19, 2017: Oncotarget
https://www.readbyqxmd.com/read/29050289/acrolein-induces-mtdna-damages-mitochondrial-fission-and-mitophagy-in-human-lung-cells
#2
Hsiang-Tsui Wang, Jing-Heng Lin, Chun-Hsiang Yang, Chun-Hao Haung, Ching-Wen Weng, Anya Maan-Yuh Lin, Yu-Li Lo, Wei-Shen Chen, Moon-Shong Tang
Acrolein (Acr), a highly reactive unsaturated aldehyde, can cause various lung diseases including asthma, chronic obstructive pulmonary disease (COPD), and lung cancer. We have found that Acr can damage not only genomic DNA but also DNA repair proteins causing repair dysfunction and enhancing cells' mutational susceptibility. While these effects may account for Acr lung carcinogenicity, the mechanisms by which Acr induces lung diseases other than cancer are unclear. In this study, we found that Acr induces damages in mitochondrial DNA (mtDNA), inhibits mitochondrial bioenergetics, and alters mtDNA copy number in human lung epithelial cells and fibroblasts...
September 19, 2017: Oncotarget
https://www.readbyqxmd.com/read/29049454/association-of-mitochondrial-dna-copy-number-with-cardiovascular-disease
#3
Foram N Ashar, Yiyi Zhang, Ryan J Longchamps, John Lane, Anna Moes, Megan L Grove, Josyf C Mychaleckyj, Kent D Taylor, Josef Coresh, Jerome I Rotter, Eric Boerwinkle, Nathan Pankratz, Eliseo Guallar, Dan E Arking
Importance: Mitochondrial dysfunction is a core component of the aging process and may play a key role in atherosclerotic cardiovascular disease. Mitochondrial DNA copy number (mtDNA-CN), which represents the number of mitochondria per cell and number of mitochondrial genomes per mitochondrion, is an indirect biomarker of mitochondrial function. Objective: To determine whether mtDNA-CN, measured in an easily accessible tissue (buffy coat/circulating leukocytes), can improve risk classification for cardiovascular disease (CVD) and help guide initiation of statin therapy for primary prevention of CVD...
October 11, 2017: JAMA Cardiology
https://www.readbyqxmd.com/read/29047204/influence-of-cell-distribution-and-diabetes-status-on-the-association-between-mitochondrial-dna-copy-number-and-aging-phenotypes-in-the-inchianti-study
#4
Ann Zenobia Moore, Jun Ding, Marcus A Tuke, Andrew R Wood, Stefania Bandinelli, Timothy M Frayling, Luigi Ferrucci
Mitochondrial DNA copy number (mtDNA-CN) estimated in whole blood is a novel marker of mitochondrial mass and function that can be used in large population-based studies. Analyses that attempt to relate mtDNA-CN to specific aging phenotypes may be confounded by differences in the distribution of blood cell types across samples. Also, low or high mtDNA-CN may have a different meaning given the presence of diseases associated with mitochondrial damage. We evaluated the impact of blood cell type distribution and diabetes status on the association between mtDNA-CN and aging phenotypes, namely chronologic age, interleukin-6, hemoglobin, and all-cause mortality, among 672 participants of the InCHIANTI study...
October 19, 2017: Aging Cell
https://www.readbyqxmd.com/read/29045673/age-related-changes-in-the-mitochondria-of-human-mural-granulosa-cells
#5
Yifan Liu, Ming Han, Xiaoshuang Li, Hui Wang, Minyue Ma, Shihui Zhang, Yifan Guo, Shuling Wang, Yuanfen Wang, N Duan, Bing Xu, Jingwen Yin, Yuanqing Yao
STUDY QUESTION: What changes in the mitochondria of human mural granulosa cells (mGCs) with maternal aging? SUMMARY ANSWER: The mitochondrial membrane potential (MMP) and the ability of oxidative phosphorylation (OXPHOS) of mGCs declines with reproductive aging, accompanied with more abnormal mitochondria. WHAT IS KNOWN ALREADY: Mitochondria play an important role in the dialogue between the mGCs and oocytes. However, the underlying mechanism of mitochondrial dysfunction in mGCs in aging is still poorly understood...
October 17, 2017: Human Reproduction
https://www.readbyqxmd.com/read/29035693/mms19-localizes-to-mitochondria-and-protects-the-mitochondrial-genome-from-oxidative-damage
#6
Rui Wu, Qunsong Tan, Kaifeng Niu, Yuqi Zhu, Di Wei, Yongliang Zhao, Hongbo Fang
MMS19 localizes to cytoplasmic and nuclear compartments involving in transcription and nucleotide excision repair (NER). However, whether or not MMS19 localizes to mitochondria where it plays a role in maintaining mitochondrial genome stability remains elusive. In this study, we provide the first evidence that MMS19 is localized in the inner membrane of mitochondria and participates in mtDNA oxidative damage repair. MMS19 knockdown led to mitochondrial dysfunctions including decreased mtDNA copy number, diminished mtDNA repair capacity and elevated level of mtDNA common deletion after oxidative stress...
October 16, 2017: Biochemistry and Cell Biology, Biochimie et Biologie Cellulaire
https://www.readbyqxmd.com/read/29030253/polymorphisms-in-the-tfam-and-pgc1-%C3%AE-genes-and-their-association-with-polycystic-ovary-syndrome-among-south-indian-women
#7
Tumu Venkat Reddy, Suresh Govatati, Mamata Deenadayal, Sisinthy Shivaji, Manjula Bhanoori
We investigated the link between polymorphisms in genes involved in mitochondrial biogenesis, mitochondrial transcription factor A (TFAM) and Peroxisome proliferator activated receptor gamma coactivator-1 alpha (PGC-1α) and further studied the role of these genes on the pathophysiology of polycystic ovary syndrome (PCOS). This case-control study was carried out in 118 PCOS cases and 110 controls. In the present study we genotyped three polymorphisms of PGC1-α gene (rs8192678-Gly482Ser, rs13131226 and rs2970856) and polymorphism of TFAM gene (rs1937-+35G/C) by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis...
October 10, 2017: Gene
https://www.readbyqxmd.com/read/29021970/quantification-of-mitochondrial-dna-copy-number-in-suspected-cancer-patients-by-a-well-optimized-ddpcr-method
#8
Ashfaque A Memon, Bengt Zöller, Anna Hedelius, Xiao Wang, Emelie Stenman, Jan Sundquist, Kristina Sundquist
Changes in mitochondrial DNA (mtDNA) content is a useful clinical biomarker for various diseases, however results are controversial as several analytical factors can affect measurement of mtDNA. MtDNA is often quantified by taking ratio between a target mitochondrial gene and a reference nuclear gene (mtDNA/nDNA) using quantitative real time PCR often on two separate experiments. It measures relative levels by using external calibrator which may not be comparable across laboratories. We have developed and optimized a droplet digital PCR (ddPCR) based method for quantification of absolute copy number of both mtDNA and nDNA gene in whole blood...
September 2017: Biomolecular Detection and Quantification
https://www.readbyqxmd.com/read/29020391/association-between-mitochondrial-dna-copy-number-and-sudden-cardiac-death-findings-from-the-atherosclerosis-risk-in-communities-study-aric
#9
Yiyi Zhang, Eliseo Guallar, Foram N Ashar, Ryan J Longchamps, Christina A Castellani, John Lane, Megan L Grove, Josef Coresh, Nona Sotoodehnia, Leonard Ilkhanoff, Eric Boerwinkle, Nathan Pankratz, Dan E Arking
Aims: Sudden cardiac death (SCD) is a major public health burden. Mitochondrial dysfunction has been implicated in a wide range of cardiovascular diseases including cardiomyopathy, heart failure, and arrhythmias, but it is unknown if it also contributes to SCD risk. We sought to examine the prospective association between mtDNA copy number (mtDNA-CN), a surrogate marker of mitochondrial function, and SCD risk. Methods and results: We measured baseline mtDNA-CN in 11 093 participants from the Atherosclerosis Risk in Communities (ARIC) study...
June 30, 2017: European Heart Journal
https://www.readbyqxmd.com/read/29018163/mtdna-copy-number-associated-with-age-of-onset-in-familial-amyloid-polyneuropathy
#10
Diana Santos, Maria João Santos, Miguel Alves-Ferreira, Teresa Coelho, Jorge Sequeiros, Isabel Alonso, Pedro Oliveira, Alda Sousa, Carolina Lemos, Manuela Grazina
BACKGROUND: Transthyretin-related familial amyloid polyneuropathy (TTR-FAP Val30Met) shows a wide variation in age-at-onset (AO) between generations and genders, as in Portuguese families, where women display a later onset and a larger anticipation (>10 years). Mitochondrial DNA (mtDNA) copy number was assessed to clarify whether it has a modifier effect on AO variability in Portuguese patients. METHODS: The mtDNA copy number of 262 samples (175 Val30Met TTR carriers and 87 controls (proven Val30Val)) was quantified by quantitative real-time PCR...
October 10, 2017: Journal of Neurology, Neurosurgery, and Psychiatry
https://www.readbyqxmd.com/read/28993480/mitochondrial-abnormality-facilitates-cyst-formation-in-autosomal-dominant-polycystic-kidney-disease
#11
Yu Ishimoto, Reiko Inagi, Daisuke Yoshihara, Masanori Kugita, Shizuko Nagao, Akira Shimizu, Norihiko Takeda, Masaki Wake, Kenjiro Honda, Jing Zhou, Masaomi Nangaku
Autosomal dominant polycystic kidney disease (ADPKD) constitutes the most common inherited kidney disease. Mutations in the PKD1 and PKD2 genes, encoding respective polycystin-1 and polycystin-2 Ca(2+) ion channels, results in tubular epithelial cell-derived renal cysts. Recent clinical studies demonstrate oxidative stress as present early in ADPKD. Mitochondria comprise the primary reactive oxygen species source and also their main effector target; however, the pathophysiological role of mitochondria in ADPKD remains uncharacterized...
October 9, 2017: Molecular and Cellular Biology
https://www.readbyqxmd.com/read/28993273/acute-mental-stress-induces-mitochondrial-bioenergetic-crisis-and-hyper-fission-along-with-aberrant-mitophagy-in-the-gut-mucosa-in-rodent-model-of-stress-related-mucosal-disease
#12
Rudranil De, Somnath Mazumder, Souvik Sarkar, Subhashis Debsharma, Asim Azhar Siddiqui, Shubhra Jyoti Saha, Chinmoy Banerjee, Shiladitya Nag, Debanjan Saha, Uday Bandyopadhyay
Psychological stress, depression and anxiety lead to multiple organ dysfunctions wherein stress-related mucosal disease (SRMD) is common to people experiencing stress and also occur as a side effect in patients admitted to intensive care units; however the underlying molecular aetiology is still obscure. We report that in rat-SRMD model, cold restraint-stress severely damaged gut mitochondrial functions to generate superoxide anion (O2(•-)), depletion of ATP and shifted mitochondrial fission-fusion dynamics towards enhanced fission to induce mucosal injury...
October 6, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28986374/chromosomal-aneuploidy-improves-brewing-characteristics-of-sake-yeast
#13
Masafumi Kadowaki, Yuki Fujimaru, Seiga Taguchi, Jannatul Ferdouse, Kazutaka Sawada, Yuta Kimura, Yohei Terasawa, Gennaro Agrimi, Toyoaki Anai, Hideki Noguchi, Atsushi Toyoda, Asao Fujiyama, Takeshi Akao, Hiroshi Kitagaki
The effect of chromosomal aneuploidy on the brewing characteristics in brewery yeasts has not been studied. Here, we report that chromosomal aneuploidy in sake brewery yeast (Saccharomyces cerevisiae) leads to the development of favorable brewing characteristics. We found that pyruvate-underproducing sake yeast, which produces less off-flavor diacetyl, is aneuploid and trisomic for chromosomes XI and XIV. To confirm that this phenotype is due to aneuploidy, we obtained 45 haploids with various chromosomal additions and investigated their brewing profiles...
October 6, 2017: Applied and Environmental Microbiology
https://www.readbyqxmd.com/read/28985301/the-trouble-with-meam2-implications-of-pseudogenes-on-species-delimitation-in-the-globally-invasive-bemisia-tabaci-hemiptera-aleyrodidae-cryptic-species-complex
#14
W T Tay, S Elfekih, L N Court, K H J Gordon, H Delatte, P J De Barro
Molecular species identification using sub-optimal PCR primers can over-estimate species diversity due to co-amplification of nuclear mitochondrial (NUMT) DNA/pseudogenes. For the agriculturally important whitefly Bemisia tabaci cryptic pest species complex, species identification depends primarily on characterisation of the mitochondrial DNA cytochrome oxidase I (mtDNA COI) gene. The lack of robust PCR primers for the mtDNA COI gene can undermine correct species identification which in turn compromises management strategies...
September 6, 2017: Genome Biology and Evolution
https://www.readbyqxmd.com/read/28982094/combined-impact-of-telomere-length-and-mitochondrial-dna-copy-number-on-cognitive-function-in-community-dwelling-very-old-adults
#15
Jee-Yon Lee, Jung-Ha Kim, Duk-Chul Lee
BACKGROUND: This study was conducted to investigate the combined impact of telomere length and mitochondrial DNA (mtDNA) copy number on cognitive function in community-dwelling very old adults. METHODS: In total, 186 subjects over 75 years participated in this study. Cognitive function was assessed using the Korean Mini-Mental State Examination, and leukocyte telomere length and mtDNA copy number were measured using real-time polymerase chain reaction methods. RESULTS: Both the fourth quartile of telomere length and mtDNA copy number were associated with cognitive dysfunction with an adjusted odds ratio of 0...
October 6, 2017: Dementia and Geriatric Cognitive Disorders
https://www.readbyqxmd.com/read/28973171/defective-mitochondrial-rrna-methyltransferase-mrm2-causes-melas-like-clinical-syndrome
#16
Caterina Garone, Aaron R D'Souza, Cristina Dallabona, Tiziana Lodi, Pedro Rebelo-Guiomar, Joanna Rorbach, Maria Alice Donati, Elena Procopio, Martino Montomoli, Renzo Guerrini, Massimo Zeviani, Sarah E Calvo, Vamsi K Mootha, Salvatore DiMauro, Ileana Ferrero, Michal Minczuk
Defects in nuclear-encoded proteins of the mitochondrial translation machinery cause early-onset and tissue-specific deficiency of one or more OXPHOS complexes. Here, we report a 7-year-old Italian boy with childhood-onset rapidly progressive encephalomyopathy and stroke-like episodes. Multiple OXPHOS defects and decreased mtDNA copy number (40%) were detected in muscle homogenate. Clinical features combined with low level of plasma citrulline were highly suggestive of mitochondrial encephalopathy, lactic acidosis and stroke-like episodes (MELAS) syndrome, however, the common m...
August 25, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28970293/mitochondrial-respiration-is-reduced-in-atherosclerosis-promoting-necrotic-core-formation-and-reducing-relative-fibrous-cap-thickness
#17
Emma P K Yu, Johannes Reinhold, Haixiang Yu, Lakshi Starks, Anna K Uryga, Kirsty Foote, Alison Finigan, Nichola Figg, Yuh-Fen Pung, Angela Logan, Michael P Murphy, Martin Bennett
OBJECTIVE: Mitochondrial DNA (mtDNA) damage is present in murine and human atherosclerotic plaques. However, whether endogenous levels of mtDNA damage are sufficient to cause mitochondrial dysfunction and whether decreasing mtDNA damage and improving mitochondrial respiration affects plaque burden or composition are unclear. We examined mitochondrial respiration in human atherosclerotic plaques and whether augmenting mitochondrial respiration affects atherogenesis. APPROACH AND RESULTS: Human atherosclerotic plaques showed marked mitochondrial dysfunction, manifested as reduced mtDNA copy number and oxygen consumption rate in fibrous cap and core regions...
September 28, 2017: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/28958595/the-mtdna-replication-related-genes-tfam-and-polg-are-associated-with-leprosy-in-han-chinese-from-southwest-china
#18
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/28944842/mitochondrial-dna%C3%A2-induced-inflammatory-damage-contributes-to-myocardial-ischemia-reperfusion-injury-in-rats-cardioprotective-role-of-epigallocatechin
#19
Chao-Yi Qin, Hong-Wei Zhang, Jun Gu, Fei Xu, Huai-Min Liang, Kang-Jun Fan, Jia-Yu Shen, Zheng-Hua Xiao, Er-Yong Zhang, Jia Hu
Inflammation serves an important role in the pathogenesis of myocardial ischemia/reperfusion (I/R) injury. Fragments of endogenous damaged‑associated molecular patterns, recently identified as mitochondrial DNA (mtDNA), have been proven to be a potent pro‑inflammatory mediator. Epigallocatechin‑3‑gallate (EGCG) is able to regulate the expression levels of a series of inflammatory cytokines. However, the involvement of endogenous mtDNA in EGCG‑regulated inflammatory activities in the context of myocardial I/R injury remains to be elucidated...
November 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28943449/inactivation-of-glycogen-synthase-kinase-3%C3%AE-gsk-3%C3%AE-enhances-skeletal-muscle-oxidative-metabolism
#20
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
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