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https://www.readbyqxmd.com/read/28205173/measurement-of-mitochondrial-cholesterol-import-using-a-mitochondria-targeted-cyp11a1-fusion-construct
#1
Barry E Kennedy, Mark Charman, Barbara Karten
All animal membranes require cholesterol as an essential regulator of biophysical properties and function, but the levels of cholesterol vary widely among different subcellular compartments. Mitochondria, and in particular the inner mitochondrial membrane, have the lowest levels of cholesterol in the cell. Nevertheless, mitochondria need cholesterol for membrane maintenance and biogenesis, as well as oxysterol, steroid, and hepatic bile acid production. Alterations in mitochondrial cholesterol have been associated with a range of pathological conditions, including cancer, hepatosteatosis, cardiac ischemia, Alzheimer's, and Niemann-Pick Type C Disease...
2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28202582/dynamic-changes-in-cardiac-mitochondrial-metabolism-during-warm-acclimation-in-rainbow-trout
#2
Nicolas Pichaud, Andreas Ekström, Kim Hellgren, Erik Sandblom
Although the mitochondrial metabolism responses to warm acclimation have been widely studied in fish, the time course of this process is less understood. Here, we characterise changes of rainbow trout (Oncorhyncus mykiss) cardiac mitochondrial metabolism during acute warming from 10 to 16°C, and during the subsequent warm acclimation for 39 days (D). We repeatedly measured mitochondrial O2 consumption in cardiac permeabilized fibers and functional integrity of mitochondria (i.e. mitochondrial coupling and cytochrome c effect) at two assay temperatures (10 and 16°C), as well as citrate synthase (CS) and lactate dehydrogenase (LDH) activities at room temperature...
February 15, 2017: Journal of Experimental Biology
https://www.readbyqxmd.com/read/28199200/mitochondrial-dna-mitochondrial-dysfunction-and-cardiac-manifestations
#3
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/28194639/ultrafine-particulate-matter-increases-cardiac-ischemia-reperfusion-injury-via-mitochondrial-permeability-transition-pore
#4
Nathan A Holland, Chad R Fraiser, Ruben C Sloan, Robert B Devlin, David A Brown, Christopher J Wingard
Ultrafine particulate matter (UFP) has been associated with increased cardiovascular morbidity and mortality. However, the mechanisms that drive PM-associated cardiovascular disease and dysfunction remain unclear. We examined the impact of oropharyngeal aspiration of 100 μg UFP from the Chapel Hill, NC, air shed in Sprague-Dawley rats on cardiac function, arrhythmogenesis, and cardiac ischemia/reperfusion (I/R) injury using a Langendorff working heart model. We found that exposure to UFP was capable of significantly exacerbating cardiac I/R injury without changing overall cardiac function or major changes in arrhythmogenesis...
February 13, 2017: Cardiovascular Toxicology
https://www.readbyqxmd.com/read/28173848/inhibition-of-dynamin-related-protein-1-protects-against-myocardial-ischemia-reperfusion-injury-in-diabetic-mice
#5
Mingge Ding, Qianqian Dong, Zhenghua Liu, Zheng Liu, Yinxian Qu, Xing Li, Cong Huo, Xin Jia, Feng Fu, Xiaoming Wang
BACKGROUND: Many cardioprotective pharmacological agents failed to exert their protective effects in diabetic hearts subjected to myocardial ischemia/reperfusion (MI/R). Identify the molecular basis linking diabetes with MI/R injury is scientifically important and may provide effective therapeutic approaches. Dynamin-related protein 1 (Drp1)-mediated mitochondrial fission plays an important role in MI/R injury under non-diabetic conditions. Importantly, recent studies indicated that Drp1-mediated mitochondrial fission is enhanced in the myocardium of diabetic mice...
February 7, 2017: Cardiovascular Diabetology
https://www.readbyqxmd.com/read/28165812/the-protective-effect-of-lipid-emulsion-in-preventing-bupivacaine-induced-mitochondrial-injury-and-apoptosis-of-h9c2-cardiomyocytes
#6
Zhe Chen, Zhousheng Jin, Yun Xia, Shishi Zhao, Xuzhong Xu, Thomas J Papadimos, Quanguang Wang
Lipid emulsion (LE) has been shown to be effective in the resuscitation of bupivacaine-induced cardiac arrest, but the precise mechanism of this action has not been fully elucidated. Pursuant to this lack of information on the mechanism in which LE protects the myocardium during bupivacaine-induced toxicity, we explored mitochondrial function and cell apoptosis. H9C2 cardiomyocytes were used in study. Cells were randomly divided in different groups and were cultivated 6 h, 12 h, and 24 h. The mitochondria were extracted and mitochondrial ATP content was measured, as was mitochondrial membrane potential, the concentration of calcium ion (Ca2+), and the activity of Ca2+-ATP enzyme (Ca2+-ATPase)...
November 2017: Drug Delivery
https://www.readbyqxmd.com/read/28160133/cardioprotective-kinase-signaling-to-subsarcolemmal-and-interfibrillar-mitochondria-is-mediated-by-caveolar-structures
#7
Wylly Ramsés García-Niño, Francisco Correa, Julia Isabel Rodríguez-Barrena, Juan Carlos León-Contreras, Mabel Buelna-Chontal, Elizabeth Soria-Castro, Rogelio Hernández-Pando, José Pedraza-Chaverri, Cecilia Zazueta
The demonstration that caveolin-3 overexpression reduces myocardial ischemia/reperfusion injury and our own finding that multiprotein signaling complexes increase in mitochondria in association with caveolin-3 levels, led us to investigate the contribution of caveolae-driven extracellular signal-regulated kinases 1/2 (ERK1/2) on maintaining the function of cardiac mitochondrial subpopulations from reperfused hearts subjected to postconditioning (PostC). Rat hearts were isolated and subjected to ischemia/reperfusion and to PostC...
March 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28158196/transcriptome-wide-co-expression-analysis-identifies-lrrc2-as-a-novel-mediator-of-mitochondrial-and-cardiac-function
#8
Chris McDermott-Roe, Marion Leleu, Glenn C Rowe, Oleg Palygin, John D Bukowy, Judy Kuo, Monika Rech, Steffie Hermans-Beijnsberger, Sebastian Schaefer, Eleonora Adami, Esther E Creemers, Matthias Heinig, Blanche Schroen, Zoltan Arany, Enrico Petretto, Aron M Geurts
Mitochondrial dysfunction contributes to myriad monogenic and complex pathologies. To understand the underlying mechanisms, it is essential to define the full complement of proteins that modulate mitochondrial function. To identify such proteins, we performed a meta-analysis of publicly available gene expression data. Gene co-expression analysis of a large and heterogeneous compendium of microarray data nominated a sub-population of transcripts that whilst highly correlated with known mitochondrial protein-encoding transcripts (MPETs), are not themselves recognized as generating proteins either localized to the mitochondrion or pertinent to functions therein...
2017: PloS One
https://www.readbyqxmd.com/read/28148493/subfunctionalization-of-cox4-paralogs-in-fish
#9
Danielle Porplycia, Gigi Y Lau, Jared McDonald, Zhilin Chen, Jeffrey G Richards, Christopher D Moyes
Cytochrome c oxidase (COX) subunit 4 has two paralogs in most vertebrates. The mammalian COX4-2 gene is hypoxia responsive and the protein has a disrupted ATP-binding site that confers kinetic properties on COX that distinguish it from COX4-1. The structure -function of COX4-2 orthologs in other vertebrates remains uncertain. Phylogenetic analyses suggest the two paralogs arose in basal vertebrates, but COX4-2 orthologs diverged faster than COX4-1 orthologs. COX4-1/4-2 protein levels in tilapia tracked mRNA levels across tissues, and did not change in hypoxia, arguing against a role for differential post-translational regulation of paralogs...
February 1, 2017: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
https://www.readbyqxmd.com/read/28139514/pim-1-kinase-regulating-dynamics-related-protein-1-mediates-sevoflurane-postconditioning-induced-cardioprotection
#10
Jin-Dong Liu, Hui-Juan Chen, Da-Liang Wang, Hui Wang, Qian Deng
BACKGROUND: It is well documented that sevoflurane postconditioning (SP) has a significant myocardial protection effect. However, the mechanisms underlying SP are still unclear. In the present study, we investigated the hypothesis that the Pim-1 kinase played a key role in SP-induced cardioprotection by regulating dynamics-related protein 1 (Drp1). METHODS: A Langendorff model was used in this study. Seventy-two rats were randomly assigned into six groups as follows: CON group, ischemia reperfusion (I/R) group, SP group , SP+proto-oncogene serine/threonine-protein kinase 1 (Pim-1) inhibitor II group, SP+dimethylsufoxide group, and Pim-1 inhibitor II group (n = 12, each)...
2017: Chinese Medical Journal
https://www.readbyqxmd.com/read/28134239/a-rab5-endosomal-pathway-mediates-parkin-dependent-mitochondrial-clearance
#11
Babette C Hammerling, Rita H Najor, Melissa Q Cortez, Sarah E Shires, Leonardo J Leon, Eileen R Gonzalez, Daniela Boassa, Sébastien Phan, Andrea Thor, Rebecca E Jimenez, Hong Li, Richard N Kitsis, Gerald W Dorn Ii, Junichi Sadoshima, Mark H Ellisman, Åsa B Gustafsson
Damaged mitochondria pose a lethal threat to cells that necessitates their prompt removal. The currently recognized mechanism for disposal of mitochondria is autophagy, where damaged organelles are marked for disposal via ubiquitylation by Parkin. Here we report a novel pathway for mitochondrial elimination, in which these organelles undergo Parkin-dependent sequestration into Rab5-positive early endosomes via the ESCRT machinery. Following maturation, these endosomes deliver mitochondria to lysosomes for degradation...
January 30, 2017: Nature Communications
https://www.readbyqxmd.com/read/28131843/inhibition-of-drp1-attenuates-mitochondrial-damage-and-myocardial-injury-in-coxsackie-virus-b3-induced-myocarditis
#12
Lin Lin, Ming Zhang, Rui Yan, Hu Shan, Jiayu Diao, Jin Wei
Viral myocarditis (VMC) is closely related to apoptosis, oxidative stress, innate immunity, and energy metabolism, which are all linked to mitochondrial dysfunction. A close nexus between mitochondrial dynamics and cardiovascular disease with mitochondrial dysfunction has been deeply researched, but there is still no relevant report in viral myocarditis. In this study, we aimed to explore the role of Dynamin-related protein 1 (Drp1)-linked mitochondrial fission in VMC. Mice were inoculated with the Coxsackie virus B3 virus (CVB3) and treated with mdivi1 (a Drp1 inhibitor)...
January 25, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28096168/sk-channel-enhancers-attenuate-ca2-dependent-arrhythmia-in-hypertrophic-hearts-by-regulating-mito-ros-dependent-oxidation-and-activity-of-ryr
#13
Tae Yun Kim, Radmila Terentyeva, Karim H F Roder, Weiyan Li, Man Liu, Ian Greener, Shanna Hamilton, Iuliia Polina, Kevin R Murphy, Richard T Clements, Samuel C Dudley, Gideon Koren, Bum-Rak Choi, Dmitry Terentyev
AIM: s: Plasmamembrane small conductance Ca<su2+p>-activated K<su+ p > (SK) channels were implicated in ventricular arrhythmias in infarcted and failing hearts. Recently, SK channels were detected in the mitochondria inner membrane (mSK), and their activation protected from acute ischemia-reperfusion injury by reducing intracellular levels of reactive oxygen species (ROS). We hypothesized that mSK play an important role in regulating mitochondrial function in chronic cardiac diseases...
January 17, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28070695/barth-syndrome-connecting-cardiolipin-to-cardiomyopathy
#14
REVIEW
Nikita Ikon, Robert O Ryan
The Barth syndrome (BTHS) is caused by an inborn error of metabolism that manifests characteristic phenotypic features including altered mitochondrial membrane phospholipids, lactic acidosis, organic acid-uria, skeletal muscle weakness and cardiomyopathy. The underlying cause of BTHS has been definitively traced to mutations in the tafazzin (TAZ) gene locus on chromosome X. TAZ encodes a phospholipid transacylase that promotes cardiolipin acyl chain remodeling. Absence of tafazzin activity results in cardiolipin molecular species heterogeneity, increased levels of monolysocardiolipin and lower cardiolipin abundance...
February 2017: Lipids
https://www.readbyqxmd.com/read/28069019/ppars-modulate-cardiac-metabolism-and-mitochondrial-function-in-diabetes
#15
REVIEW
Ting-Wei Lee, Kuan-Jen Bai, Ting-I Lee, Tze-Fan Chao, Yu-Hsun Kao, Yi-Jen Chen
Diabetic cardiomyopathy is a major complication of diabetes mellitus (DM). Currently, effective treatments for diabetic cardiomyopathy are limited. The pathophysiology of diabetic cardiomyopathy is complex, whereas mitochondrial dysfunction plays a vital role in the genesis of diabetic cardiomyopathy. Metabolic regulation targeting mitochondrial dysfunction is expected to be a reasonable strategy for treating diabetic cardiomyopathy. Peroxisome proliferator-activated receptors (PPARs) are master executors in regulating glucose and lipid homeostasis and also modulate mitochondrial function...
January 10, 2017: Journal of Biomedical Science
https://www.readbyqxmd.com/read/28051329/regulation-of-the-cardioprotective-adiponectin-and-its-receptor-adipor1-by-salt
#16
Nicholas Arnold, Abuzar Mahmood, Maya Ramdas, Paul P Ehlinger, Lakshmi Pulakat
Both circulating adiponectin (APN) and cardiac APN exert cardioprotective effects and improve insulin sensitivity and mitochondrial function. Low circulating APN serves as a biomarker for cardiovascular risk. Ablation of adiponectin receptor 1 (AdipoR1) causes myocardial mitochondrial dysfunction. Although high salt intake is a contributor to cardiovascular disease, how it modulates the expression of APN or AdipoR1 in cardiomyocytes is not known. We report that APN mRNA expression was attenuated in a dose-dependent manner in mouse cardiomyocyte cell line HL-1 exposed to salt concentrations ranging from 0...
November 30, 2016: Canadian Journal of Physiology and Pharmacology
https://www.readbyqxmd.com/read/28051130/the-histone-3-lysine-9-methyltransferase-inhibitor-chaetocin-improves-prognosis-in-a-rat-model-of-high-salt-diet-induced-heart-failure
#17
Tomohiko Ono, Naomi Kamimura, Tomohiro Matsuhashi, Toshihiro Nagai, Takahiko Nishiyama, Jin Endo, Takako Hishiki, Tsuyoshi Nakanishi, Noriaki Shimizu, Hirotoshi Tanaka, Shigeo Ohta, Makoto Suematsu, Masaki Ieda, Motoaki Sano, Keiichi Fukuda, Ruri Kaneda
Histone acetylation has been linked to cardiac hypertrophy and heart failure. However, the pathological implications of changes in histone methylation and the effects of interventions with histone methyltransferase inhibitors for heart failure have not been fully clarified. Here, we focused on H3K9me3 status in the heart and investigated the effects of the histone H3K9 methyltransferase inhibitor chaetocin on prognoses in Dahl salt-sensitive rats, an animal model of chronic heart failure. Chaetocin prolonged survival and restored mitochondrial dysfunction...
January 4, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28034298/effective-agents-targeting-the-mitochondria-and-apoptosis-to-protect-the-heart
#18
Eltyeb Abdelwahid, Aurimas Stulpinas, Audrone Kalvelyte
A wide variety of agents have been traditionally used in cardiovascular medicine worldwide and their precise mechanisms of action have been demonstrated to be largely related to the cardiomyocyte mitochondria and apoptosis. Abnormalities in the structure and function of the mitochondria and mutations in mitochondrial DNA can decrease energy production, alter the redox system, impair calcium homeostasis, and induce the mitochondrial permeability transition pore (MPTP), causing cell death. All of these data provide evidence of mitochondrial signaling pathways as targets to downregulate cardiac cell apoptosis and thus to prevent and treat cardiovascular diseases...
December 29, 2016: Current Pharmaceutical Design
https://www.readbyqxmd.com/read/28008641/effects-of-mirnas-on-myocardial-apoptosis-by-modulating-mitochondria-related-proteins
#19
REVIEW
Yanfang Zhao, Murugavel Ponnusamy, Yanhan Dong, Lei Zhang, Kun Wang, Peifeng Li
Myocardial apoptosis play a vital role in pathogenesis of cardiovascular diseases. The intrinsic pathway of apoptosis (mitochondrial apoptosis pathway) and abnormal mitochondrial fission and fusion have a detrimental effect on cells under a variety of intracellular stresses including hypoxia, oxidative stress, drug toxicity or DNA damage and contributes to the development of heart failure (HF), myocardial infarction (MI), diabetic cardiomyopathy and ischemia/reperfusion injury (I/R). MicroRNAs (miRNAs) are endogenous short noncoding RNAs, which target 3'-untranslated region of mRNA to switch off gene expression...
December 23, 2016: Clinical and Experimental Pharmacology & Physiology
https://www.readbyqxmd.com/read/28004807/expert-consensus-document-mitochondrial-function-as-a-therapeutic-target-in-heart-failure
#20
David A Brown, Justin B Perry, Mitchell E Allen, Hani N Sabbah, Brian L Stauffer, Saame Raza Shaikh, John G F Cleland, Wilson S Colucci, Javed Butler, Adriaan A Voors, Stefan D Anker, Bertram Pitt, Burkert Pieske, Gerasimos Filippatos, Stephen J Greene, Mihai Gheorghiade
Heart failure is a pressing worldwide public-health problem with millions of patients having worsening heart failure. Despite all the available therapies, the condition carries a very poor prognosis. Existing therapies provide symptomatic and clinical benefit, but do not fully address molecular abnormalities that occur in cardiomyocytes. This shortcoming is particularly important given that most patients with heart failure have viable dysfunctional myocardium, in which an improvement or normalization of function might be possible...
December 22, 2016: Nature Reviews. Cardiology
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