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https://www.readbyqxmd.com/read/28539870/a-select-subset-of-electron-transport-chain-genes-associated-with-optic-atrophy-link-mitochondria-to-axon-regeneration-in-caenorhabditis-elegans
#1
Wendy M Knowlton, Thomas Hubert, Zilu Wu, Andrew D Chisholm, Yishi Jin
The role of mitochondria within injured neurons is an area of active interest since these organelles are vital for the production of cellular energy in the form of ATP. Using mechanosensory neurons of the nematode Caenorhabditis elegans to test regeneration after neuronal injury in vivo, we surveyed genes related to mitochondrial function for effects on axon regrowth after laser axotomy. Genes involved in mitochondrial transport, calcium uptake, mitophagy, or fission and fusion were largely dispensable for axon regrowth, with the exception of eat-3/Opa1...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/28536949/exercise-and-doxorubicin-treatment-modulate-cardiac-mitochondrial-quality-control-signaling
#2
I Marques-Aleixo, E Santos-Alves, J R Torrella, P J Oliveira, J Magalhães, A Ascensão
The cross-tolerance effect of exercise against heart mitochondrial-mediated quality control, remodeling and death-related mechanisms associated with sub-chronic Doxorubicin (DOX) treatment is yet unknown. We therefore analyzed the effects of two distinct chronic exercise models (endurance treadmill training-TM and voluntary free wheel activity-FW) performed during the course of the sub-chronic DOX treatment on mitochondrial susceptibility to permeability transition pore (mPTP), apoptotic and autophagic signaling and mitochondrial dynamics...
May 23, 2017: Cardiovascular Toxicology
https://www.readbyqxmd.com/read/28503736/hydrogen-sulfide-pretreatment-improves-mitochondrial-function-in-myocardial-hypertrophy-via-a-sirt3-dependent-manner
#3
Guoliang Meng, Jieqiong Liu, Shangmin Liu, Qiuyi Song, Lulu Liu, Liping Xie, Yi Han, Yong Ji
BACKGROUND AND PURPOSE Hydrogen sulfide (H2 S) is a gaseous signal molecule with anti-oxidative ability. Sirtuin 3 (SIRT3) is closely associated with mitochondrial function and oxidative stress. The study was to investigate whether and how H2 S improved myocardial hypertrophy via a SIRT3-dependent manner. EXPERIMENTAL APPROACH Neonatal rat cardiomyocytes were pre-treated with NaHS (50 μM) for 4 h followed by angiotensin II (Ang II, 100 nM) for 24 h. SIRT3 was silenced with siRNA technology. SIRT 3 promoter activity and expression, cell surface, hypertrophic gene mRNA expression, mitochondrial oxygen consumption rate and membrane potential were measured...
May 15, 2017: British Journal of Pharmacology
https://www.readbyqxmd.com/read/28494813/not-only-dominant-not-only-optic-atrophy-expanding-the-clinical-spectrum-associated-with-opa1-mutations
#4
Alessia Nasca, Teresa Rizza, Mara Doimo, Andrea Legati, Andrea Ciolfi, Daria Diodato, Cristina Calderan, Gianfranco Carrara, Eleonora Lamantea, Chiara Aiello, Michela Di Nottia, Marcello Niceta, Costanza Lamperti, Anna Ardissone, Stefania Bianchi-Marzoli, Giancarlo Iarossi, Enrico Bertini, Isabella Moroni, Marco Tartaglia, Leonardo Salviati, Rosalba Carrozzo, Daniele Ghezzi
BACKGROUND: Heterozygous mutations in OPA1 are a common cause of autosomal dominant optic atrophy, sometimes associated with extra-ocular manifestations. Few cases harboring compound heterozygous OPA1 mutations have been described manifesting complex neurodegenerative disorders in addition to optic atrophy. RESULTS: We report here three patients: one boy showing an early-onset mitochondrial disorder with hypotonia, ataxia and neuropathy that was severely progressive, leading to early death because of multiorgan failure; two unrelated sporadic girls manifesting a spastic ataxic syndrome associated with peripheral neuropathy and, only in one, optic atrophy...
May 12, 2017: Orphanet Journal of Rare Diseases
https://www.readbyqxmd.com/read/28473727/cryptolepine-inhibits-melanoma-cell-growth-through-coordinated-changes-in-mitochondrial-biogenesis-dynamics-and-metabolic-tumor-suppressor-ampk%C3%AE-1-2-lkb1
#5
Harish C Pal, Ram Prasad, Santosh K Katiyar
Dysregulated mitochondrial dynamics and biogenesis have been associated with various pathological conditions including cancers. Here, we assessed the therapeutic effect of cryptolepine, a pharmacologically active alkaloid derived from the roots of Cryptolepis sanguinolenta, on melanoma cell growth. Treatment of human melanoma cell lines (A375, Hs294t, SK-Mel28 and SK-Mel119) with cryptolepine (1.0, 2.5, 5.0 and 7.5 μM) for 24 and 48 h significantly (P < 0.001) inhibited the growth of melanoma cells but not normal melanocytes...
May 4, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28463235/perturbations-in-the-apoptotic-pathway-and-mitochondrial-network-dynamics-in-peripheral-blood-mononuclear-cells-from-bipolar-disorder-patients
#6
G Scaini, G R Fries, S S Valvassori, C P Zeni, G Zunta-Soares, M Berk, J C Soares, J Quevedo
Bipolar disorder (BD) is a severe psychiatric disorder characterized by phasic changes of mood and can be associated with progressive structural brain change and cognitive decline. The numbers and sizes of glia and neurons are reduced in several brain areas, suggesting the involvement of apoptosis in the pathophysiology of BD. Because the changes in mitochondrial dynamics are closely related with the early process of apoptosis and the specific processes of apoptosis and mitochondrial dynamics in BD have not been fully elucidated, we measured the apoptotic pathway and the expression of mitochondrial fission/fusion proteins from BD patients and healthy controls...
May 2, 2017: Translational Psychiatry
https://www.readbyqxmd.com/read/28442211/leigh-like-neuroimaging-features-associated-with-new-biallelic-mutations-in-opa1
#7
Anna Rubegni, Tiziana Pisano, Giacomo Bacci, Alessandra Tessa, Roberta Battini, Elena Procopio, Sabrina Giglio, Rosa Pasquariello, Filippo Maria Santorelli, Renzo Guerrini, Claudia Nesti
Behr syndrome is characterized by the association of early onset optic atrophy, cerebellar ataxia, pyramidal signs, peripheral neuropathy and mental retardation. Recently, some cases were reported to be caused by biallelic mutations in OPA1. We describe an 11-year-old girl (Pt1) and a 7-year-old boy (Pt2) with cognitive delay, ataxic gait and clinical signs suggestive of a peripheral neuropathy, with onset in early infancy. In Pt1 ocular fundus examination revealed optic disk pallor whereas Pt2 exhibited severe optic atrophy...
April 15, 2017: European Journal of Paediatric Neurology: EJPN
https://www.readbyqxmd.com/read/28427098/opa1-in-lipid-metabolism-function-of-opa1-in-lipolysis-and-thermogenesis-of-adipocytes
#8
Dinh-Toi Chu, Yang Tao, Kjetil Taskén
OPA1 (Optic Atrophy 1) is a mitochondrial GTPase known to regulate fission of mitochondria. It was recently also shown to locate on lipid droplets in adipocytes where it functions as an A-kinase anchoring protein (AKAP) that mediates adrenergic control of lipolysis by facilitating PKA phosphorylation of perilipin (Plin1). In brown adipocytes indirect evidence support the notion that OPA1 regulation of fission serves to increase thermogenesis, which thereby contributes to dissipation of energy. In white adipocytes, OPA1 located on lipid droplets serves as a gatekeeper to control lipolysis induced by adrenergic agonists...
April 2017: Hormone and Metabolic Research, Hormon- und Stoffwechselforschung, Hormones et Métabolisme
https://www.readbyqxmd.com/read/28423551/metabolic-reprogramming-of-the-premalignant-colonic-mucosa-is-an-early-event-in-carcinogenesis
#9
Mart Dela Cruz, Sarah Ledbetter, Sanjib Chowdhury, Ashish K Tiwari, Navneet Momi, Ramesh K Wali, Charles Bliss, Christopher Huang, David Lichtenstein, Swati Bhattacharya, Anisha Varma-Wilson, Vadim Backman, Hemant K Roy
BACKGROUND: Colorectal cancer (CRC) is the second leading cause of cancer-related mortality in the United States. There is an increasing need for the identification of biomarkers of pre-malignant and early stage CRC to improve risk-stratification and screening recommendations. In this study, we investigated the possibility of metabolic and mitochondrial reprogramming early in the pre-malignant colorectal field. METHODS: Rectal biopsies were taken from 81 patients undergoing screening colonoscopy, and gene expression of metabolic and mitochondrial markers were assessed using real time quantitative PCR...
March 28, 2017: Oncotarget
https://www.readbyqxmd.com/read/28410195/antagonistic-effects-of-selenium-on-lead-induced-autophagy-by-influencing-mitochondrial-dynamics-in-the-spleen-of-chickens
#10
Yujing Han, Chunqiu Li, Mingjun Su, Zhihui Wang, Ning Jiang, Dongbo Sun
Lead (Pb) may damage the immune function in human and animal. Selenium (Se) has antagonistic effects on Pb. In our study, brown layer chickens were randomly allocated to control group, Se group (1 mg/kg Se), Se+Pb group (1 mg/kg Se and 350 mg/kg Pb), and Pb group (350 mg/kg Pb). The chickens were sacrificed on the 90th day; spleen tissues were subjected to observation of ultrastructure and detection of spleen-related indexes. The results revealed that in the Pb group, expression levels of the cytokines IL-1 and TNF-α significantly increased, and expression levels of IL-2 and INF-γ significantly decreased; activities of antioxidant enzyme GPX, SOD and CAT significantly decreased, and expression level of malondialdehyde (MDA) significantly increased; expression levels of mitochondrial fission-related genes (Mff and Drp1) significantly increased, and expression levels of mitochondrial fusion-related genes (Opa1, Mfn1 and Mfn2) significantly decreased; expression of autophagy-related genes (Beclin 1, Dynein, Atg 5, LC3-I and LC-II) was upregulated, while expression of mammalian target of rapamycin (mTOR) was downregulated...
May 16, 2017: Oncotarget
https://www.readbyqxmd.com/read/28379197/abnormalities-of-mitochondrial-dynamics-in-neurodegenerative-diseases
#11
REVIEW
Ju Gao, Luwen Wang, Jingyi Liu, Fei Xie, Bo Su, Xinglong Wang
Neurodegenerative diseases are incurable and devastating neurological disorders characterized by the progressive loss of the structure and function of neurons in the central nervous system or peripheral nervous system. Mitochondria, organelles found in most eukaryotic cells, are essential for neuronal survival and are involved in a number of neuronal functions. Mitochondrial dysfunction has long been demonstrated as a common prominent early pathological feature of a variety of common neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and Huntington's disease (HD)...
April 5, 2017: Antioxidants (Basel, Switzerland)
https://www.readbyqxmd.com/read/28378518/autophagy-controls-the-pathogenicity-of-opa1-mutations-in-dominant-optic-atrophy
#12
Mariame Selma Kane, Jennifer Alban, Valérie Desquiret-Dumas, Naïg Gueguen, Layal Ishak, Marc Ferre, Patrizia Amati-Bonneau, Vincent Procaccio, Dominique Bonneau, Guy Lenaers, Pascal Reynier, Arnaud Chevrollier
Optic Atrophy 1 (OPA1) gene mutations cause diseases ranging from isolated dominant optic atrophy (DOA) to various multisystemic disorders. OPA1, a large GTPase belonging to the dynamin family, is involved in mitochondrial network dynamics. The majority of OPA1 mutations encodes truncated forms of the protein and causes DOA through haploinsufficiency, whereas missense OPA1 mutations are predicted to cause disease through deleterious dominant-negative mechanisms. We used 3D imaging and biochemical analysis to explore autophagy and mitophagy in fibroblasts from seven patients harbouring OPA1 mutations...
April 4, 2017: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/28342806/molecular-regulation-of-mitochondrial-dynamics-in-cardiac-disease
#13
REVIEW
Jinliang Nan, Wei Zhu, M S Rahman, Mingfei Liu, Dan Li, Shengan Su, Na Zhang, Xinyang Hu, Hong Yu, Mahesh P Gupta, Jian'an Wang
Mitochondrial homeostasis is critical for keeping functional heart in response to metabolic or environmental stresses. Mitochondrial fission and fusion (mitochondrial dynamics) play essential roles in maintaining mitochondrial homeostasis, defects in mitochondrial dynamics lead to cardiac diseases such as ischemia-reperfusion injury (IRI), heart failure and diabetic cardiomyopathy. Mitochondrial dynamics is determined by mitochondrial fission and fusion proteins, including OPA1, mitofusins and Drp1. These proteins are tightly regulated by a series of signaling pathways through different aspects such as transcription, post translation modifications (PTMs) and proteasome-dependent protein degradation...
March 22, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28298442/the-short-variant-of-the-mitochondrial-dynamin-opa1-maintains-mitochondrial-energetics-and-cristae-structure
#14
Hakjoo Lee, Sylvia B Smith, Yisang Yoon
The protein optic atrophy 1 (OPA1) is a dynamin-related protein associated with the inner mitochondrial membrane and functions in mitochondrial inner membrane fusion and cristae maintenance. Inner membrane-anchored long OPA1 (L-OPA1) undergoes proteolytic cleavage resulting in short OPA1 (S-OPA1). It is often thought that S-OPA1 is a functionally insignificant proteolytic product of L-OPA1 because the accumulation of S-OPA1 due to L-OPA1 cleavage is observed in mitochondrial fragmentation and dysfunction. However, cells contain a mixture of both L- and S-OPA1 in normal conditions, suggesting the functional significance of maintaining both OPA1 forms, but the differential roles of L- and S-OPA1 in mitochondrial fusion and energetics are ill-defined...
April 28, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28290498/inhibition-of-leukotriene-b4-receptor-1-attenuates-lipopolysaccharide-induced-cardiac-dysfunction-role-of-ampk-regulated-mitochondrial-function
#15
Meng Sun, Rui Wang, Qinghua Han
Leukotriene B4 (LTB4)-mediated leukocyte recruitment and inflammatory cytokine production make crucial contributions to chronic inflammation and sepsis; however, the role of LTB4 in lipopolysaccharide (LPS)-induced cardiac dysfunction remains unclear. Therefore, the present study addressed this issue using an LTB4 receptor 1 (BLT1) inhibitor. Administration of LPS to mice resulted in decreased cardiovascular function. Inhibition of LTB4/BLT1 with the BLT1 inhibitor U75302 significantly improved survival and attenuated the LPS-induced acute cardiac dysfunction...
March 14, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28288130/parl-mediates-smac-proteolytic-maturation-in-mitochondria-to-promote-apoptosis
#16
Shotaro Saita, Hendrik Nolte, Kai Uwe Fiedler, Hamid Kashkar, A Saskia Venne, René P Zahedi, Marcus Krüger, Thomas Langer
Mitochondria drive apoptosis by releasing pro-apoptotic proteins that promote caspase activation in the cytosol. The rhomboid protease PARL, an intramembrane cleaving peptidase in the inner membrane, regulates mitophagy and plays an ill-defined role in apoptosis. Here, we employed PARL-based proteomics to define its substrate spectrum. Our data identified the mitochondrial pro-apoptotic protein Smac (also known as DIABLO) as a PARL substrate. In apoptotic cells, Smac is released into the cytosol and promotes caspase activity by inhibiting inhibitors of apoptosis (IAPs)...
March 13, 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/28251677/mitochondrial-dna-and-primary-mitochondrial-dysfunction-in-parkinson-s-disease
#17
REVIEW
Maria Pia Giannoccaro, Chiara La Morgia, Giovanni Rizzo, Valerio Carelli
In 1979, it was observed that parkinsonism could be induced by a toxin inhibiting mitochondrial respiratory complex I. This initiated the long-standing hypothesis that mitochondrial dysfunction may play a key role in the pathogenesis of Parkinson's disease (PD). This hypothesis evolved, with accumulating evidence pointing to complex I dysfunction, which could be caused by environmental or genetic factors. Attention was focused on the mitochondrial DNA, considering the occurrence of mutations, polymorphic haplogroup-specific variants, and defective mitochondrial DNA maintenance with the accumulation of multiple deletions and a reduction of copy number...
March 2, 2017: Movement Disorders: Official Journal of the Movement Disorder Society
https://www.readbyqxmd.com/read/28245802/characterization-of-two-novel-intronic-opa1-mutations-resulting-in-aberrant-pre-mrna-splicing
#18
Ramona Bolognini, Christina Gerth-Kahlert, Mathias Abegg, Deborah Bartholdi, Nicolas Mathis, Veit Sturm, Sabina Gallati, André Schaller
BACKGROUND: We report two novel splice region mutations in OPA1 in two unrelated families presenting with autosomal-dominant optic atrophy type 1 (ADOA1) (ADOA or Kjer type optic atrophy). Mutations in OPA1 encoding a mitochondrial inner membrane protein are a major cause of ADOA. METHODS: We analyzed two unrelated families including four affected individuals clinically suspicious of ADOA. Standard ocular examinations were performed in affected individuals of both families...
February 28, 2017: BMC Medical Genetics
https://www.readbyqxmd.com/read/28239650/mitophagy-and-mitochondrial-biogenesis-in-atrial-tissue-of-patients-undergoing-heart-surgery-with-cardiopulmonary-bypass
#19
Allen M Andres, Kyle C Tucker, Amandine Thomas, David J R Taylor, David Sengstock, Salik M Jahania, Reza Dabir, Somayeh Pourpirali, Jamelle A Brown, David G Westbrook, Scott W Ballinger, Robert M Mentzer, Roberta A Gottlieb
Mitophagy occurs during ischemia/reperfusion (I/R) and limits oxidative stress and injury. Mitochondrial turnover was assessed in patients undergoing cardiac surgery involving cardiopulmonary bypass (CPB). Paired biopsies of right atrial appendage before initiation and after weaning from CPB were processed for protein analysis, mitochondrial DNA/nuclear DNA ratio (mtDNA:nucDNA ratio), mtDNA damage, mRNA, and polysome profiling. Mitophagy in the post-CPB samples was evidenced by decreased levels of mitophagy adapters NDP52 and optineurin in whole tissue lysate, decreased Opa1 long form, and translocation of Parkin to the mitochondrial fraction...
February 23, 2017: JCI Insight
https://www.readbyqxmd.com/read/28228254/control-of-mitochondrial-remodeling-by-the-atpase-inhibitory-factor-1%C3%A2-unveils-a-pro-survival-relay-via-opa1
#20
Danilo Faccenda, Junji Nakamura, Giulia Gorini, Gurtej K Dhoot, Mauro Piacentini, Masusuke Yoshida, Michelangelo Campanella
The ubiquitously expressed ATPase inhibitory factor 1 (IF1) is a mitochondrial protein that blocks the reversal of the F1Fo-ATPsynthase, preventing dissipation of cellular ATP and ischemic damage. IF1 suppresses programmed cell death, enhancing tumor invasion and chemoresistance, and is expressed in various types of human cancers. In this study, we examined its effect on mitochondrial redox balance and apoptotic cristae remodeling, finding that, by maintaining ATP levels, IF1 reduces glutathione (GSH) consumption and inactivation of peroxiredoxin 3 (Prx3) during apoptosis...
February 21, 2017: Cell Reports
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