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https://www.readbyqxmd.com/read/28716666/mouse-cardiac-mitochondria-do-not-separate-in-subsarcolemmal-and-interfibrillar-subpopulations
#1
Ulrike B Hendgen-Cotta, Sonja Esfeld, Holger Jastrow, Matthias Totzeck, Joachim Altschmied, Christine Goy, Judith Haendeler, Elke Winterhager, Tienush Rassaf
Cardiomyocytes consist of longitudinally oriented myofibril bundles with a misaligned composition caused by the uneven contours of the intercalated discs. The cytoplasmic space harbors the organelles, including mitochondria. This study investigated whether cardiomyocytes contain spatially and ultrastructurally discrete pools of mitochondria that can be separated for structurally and functionally appraisal in (patho)physiology. Transmission electron microscopy disclosed continuous transitions of mitochondria without attributable characteristics from beneath the sarcolemma directly into the barrier-free cytoplasmic space between myofibrils...
July 14, 2017: Mitochondrion
https://www.readbyqxmd.com/read/28713289/mitochondrial-vdac1-a-key-gatekeeper-as-potential-therapeutic-target
#2
REVIEW
Amadou K S Camara, YiFan Zhou, Po-Chao Wen, Emad Tajkhorshid, Wai-Meng Kwok
Mitochondria are the key source of ATP that fuels cellular functions, and they are also central in cellular signaling, cell division and apoptosis. Dysfunction of mitochondria has been implicated in a wide range of diseases, including neurodegenerative and cardiac diseases, and various types of cancer. One of the key proteins that regulate mitochondrial function is the voltage-dependent anion channel 1 (VDAC1), the most abundant protein on the outer membrane of mitochondria. VDAC1 is the gatekeeper for the passages of metabolites, nucleotides, and ions; it plays a crucial role in regulating apoptosis due to its interaction with apoptotic and anti-apoptotic proteins, namely members of the Bcl-2 family of proteins and hexokinase...
2017: Frontiers in Physiology
https://www.readbyqxmd.com/read/28709769/exploring-the-mitochondrial-microrna-import-pathway-through-polynucleotide-phosphorylase-pnpase
#3
Danielle L Shepherd, Quincy A Hathaway, Mark V Pinti, Cody E Nichols, Andrya J Durr, Shruthi Sreekumar, Kristen M Hughes, Seth M Stine, Ivan Martinez, John M Hollander
Cardiovascular disease is the primary cause of mortality for individuals with type 2 diabetes mellitus. During the diabetic condition, cardiovascular dysfunction can be partially attributed to molecular changes in the tissue, including alterations in microRNA (miRNA) interactions. MiRNAs have been reported in the mitochondrion and their presence may influence cellular bioenergetics, creating decrements in functional capacity. In this study, we examined the roles of Argonaute 2 (Ago2), a protein associated with cytosolic and mitochondrial miRNAs, and Polynucleotide Phosphorylase (PNPase), a protein found in the inner membrane space of the mitochondrion, to determine their role in mitochondrial miRNA import...
July 11, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28707980/extranuclear-sirtuins-and-metabolic-stress
#4
Mahmoud Sobhy Elkhwanky, Jukka Hakkola
SIGNIFICANCE: Extranuclear sirtuins in cytosol (SIRT2) and mitochondria (SIRT3, SIRT4 and SIRT5) are key regulators of metabolic enzymes and the antioxidative defense mechanisms. They play an important role in the adjustment of metabolic pathways in alterations of the nutritional status. Recent Advances: Recent studies have shown that in addition to lysine deacetylation, sirtuins catalyze several different lysine deacylation reactions, removal of lipid modifications and ADP-ribosylation...
July 14, 2017: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/28707739/angiotensin-ii-preconditioning-is-associated-with-increased-pkc%C3%AE%C2%B5-pkc%C3%AE-ratio-and-prosurvival-kinases-in-mitochondria
#5
Rebeca E Nuñez, Sabzali Javadov, Nelson Escobales
Angiotensin II preconditioning (APC) has been shown to reproduce the cardioprotective effects of ischaemic preconditioning (IPC), however, molecular mechanisms mediating the effects of APC remain unknown. In this study, Langendorff-perfused rat hearts were subjected to IPC, APC or both (IPC/APC) followed by ischaemia-reperfusion (IR), to determine translocation of PKCε, PKCδ, Akt, Erk1/2, JNK, p38 MAPK and GSK-3β to mitochondria as an indicator of activation of the protein kinases. In agreement with previous observations, IPC, APC and IPC/APC increased the recovery of left ventricular developed pressure (LVDP), reduced infarct size (IS) and lactate dehydrogenase (LDH) release, compared to controls...
July 14, 2017: Clinical and Experimental Pharmacology & Physiology
https://www.readbyqxmd.com/read/28705612/cardiac-mitochondrial-dynamics-mir-mediated-regulation-during-cardiac-injury
#6
Anusha Sivakumar, Ramasamy Subbiah, Rekha Balakrishnan, Jeyaprakash Rajendhran
Mitochondrial integrity is indispensable for cardiac health. With the advent of modern imaging technologies, mitochondrial motility and dynamics within the cell are extensively studied. Terminally differentiated and well-structured cardiomyocytes depict little mitochondrial division and fusion, questioning the contribution of mitochondrial fusion proteins (Mitofusin 1/2 and Optic Atrophy 1 protein) and fission factors (Dynamin-like protein 1 and mitochondrial fission 1 protein) in cardiomyocyte homeostasis...
July 10, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28703803/micu1-protects-against-myocardial-ischemia-reperfusion-injury-and-its-control-by-the-importer-receptor-tom70
#7
Qiang Xue, Haifeng Pei, Qinshe Liu, Mingjun Zhao, Jing Sun, Erhe Gao, Xinliang Ma, Ling Tao
Mitochondrial Ca(2+) overload is a main contributor to mitochondrial damage hence cardiomyocyte death in myocardial ischemia/reperfusion (MI/R) injury. MICU1 has been recently identified as an important regulator of mitochondrial Ca(2+) homeostasis. Here we try to identify the role of MICU1 in MI/R, and to investigate whether the mitochondrial importer receptor Tom70 possesses critical roles in the mitochondrial translocation of MICU1 and MI/R. Specific small interfering RNA (20 μg) against MICU1 and Tom70, and lentivirus vectors carrying the Tom70a sequences (3...
July 13, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28700655/cyclophosphamide-leads-to-persistent-deficits-in-physical-performance-and-in-vivo-mitochondria-function-in-a-mouse-model-of-chemotherapy-late-effects
#8
Marie-Laure Crouch, Gary Knowels, Rudolph Stuppard, Nolan G Ericson, Jason H Bielas, David J Marcinek, Karen L Syrjala
Fatigue is the symptom most commonly reported by long-term cancer survivors and is increasingly recognized as related to skeletal muscle dysfunction. Traditional chemotherapeutic agents can cause acute toxicities including cardiac and skeletal myopathies. To investigate the mechanism by which chemotherapy may lead to persistent skeletal muscle dysfunction, mature adult mice were injected with a single cyclophosphamide dose and evaluated for 6 weeks. We found that exposed mice developed a persistent decrease in treadmill running time compared to baseline (25...
2017: PloS One
https://www.readbyqxmd.com/read/28695818/progress-in-molecular-genetic-study-of-mitochondrial-cardiomyopathy
#9
Ruiqi Zhuge, Rong Zhou, Xinhai Ni
Mitochondria plays a key role in providing ATP for the energy-consuming cardiac tissues. Mitochondrial cardiomyopathy is a myocardial condition characterized by abnormal heart structure and/or function secondary to genetic defects involving the mitochondrial respiratory chain. The typical cardiac manifestations of mitochondrial cardiomyopathy include hypertrophic and dilated cardiomyopathy,while left ventricular myocardial noncompaction is less common. Recent research has suggested that most mitochondrial diseases result from mitochondrial DNA mutation,which can be found in genes that encode ancillary proteins needed for genetic transcription (tRNA),in genes that encode subunits of the electron transport chain complexes,or in genes that control the activities of the mitochondria called D-loop zone...
June 20, 2017: Zhongguo Yi Xue Ke Xue Yuan Xue Bao. Acta Academiae Medicinae Sinicae
https://www.readbyqxmd.com/read/28692422/mitochondrial-flashes-regulate-atp-homeostasis-in-the-heart
#10
Xianhua Wang, Xing Zhang, Di Wu, Zhanglong Huang, Tingting Hou, Chongshu Jian, Peng Yu, Fujian Lu, Rufeng Zhang, Tao Sun, Jinghang Li, Wenfeng Qi, Yanru Wang, Feng Gao, Heping Cheng
The maintenance of a constant ATP level ('set-point') is a vital homeostatic function shared by eukaryotic cells. In particular, mammalian myocardium exquisitely safeguards its ATP set-point despite 10-fold fluctuations in cardiac workload. However, the exact mechanisms underlying this regulation of ATP homeostasis remain elusive. Here we show mitochondrial flashes (mitoflashes), recently discovered dynamic activity of mitochondria, play an essential role for the auto-regulation of ATP set-point in the heart...
July 10, 2017: ELife
https://www.readbyqxmd.com/read/28685325/potential-signaling-pathways-of-acute-endurance-exercise-induced-cardiac-autophagy-and-mitophagy-and-its-possible-role-in-cardioprotection
#11
REVIEW
Youngil Lee, Insu Kwon, Yongchul Jang, Wankeun Song, Ludmila M Cosio-Lima, Mark H Roltsch
Cardiac myocytes are terminally differentiated cells and possess extremely limited regenerative capacity; therefore, preservation of mature cardiac myocytes throughout the individual's entire life span contributes substantially to healthy living. Autophagy, a lysosome-dependent cellular catabolic process, is essential for normal cardiac function and mitochondria maintenance. Therefore, it may be reasonable to hypothesize that if endurance exercise promotes cardiac autophagy and mitochondrial autophagy or mitophagy, exercise-induced cardiac autophagy (EICA) or exercise-induced cardiac mitophagy (EICM) may confer propitious cellular environment and thus protect the heart against detrimental stresses, such as an ischemia-reperfusion (I/R) injury...
July 6, 2017: Journal of Physiological Sciences: JPS
https://www.readbyqxmd.com/read/28684623/calcium-and-excitation-contraction-coupling-in-the-heart
#12
REVIEW
David A Eisner, Jessica L Caldwell, Kornél Kistamás, Andrew W Trafford
Cardiac contractility is regulated by changes in intracellular Ca concentration ([Ca(2+)]i). Normal function requires that [Ca(2+)]i be sufficiently high in systole and low in diastole. Much of the Ca needed for contraction comes from the sarcoplasmic reticulum and is released by the process of calcium-induced calcium release. The factors that regulate and fine-tune the initiation and termination of release are reviewed. The precise control of intracellular Ca cycling depends on the relationships between the various channels and pumps that are involved...
July 7, 2017: Circulation Research
https://www.readbyqxmd.com/read/28681086/effect-of-low-level-laser-treated-mesenchymal-stem-cells-on-myocardial-infarction
#13
Zaynab H El Gammal, Amr M Zaher, Nagwa El-Badri
Cardiovascular disease is the leading cause of death worldwide. Although cardiac transplantation is considered the most effective therapy for end-stage cardiac diseases, it is limited by the availability of matching donors and the complications of the immune suppressive regimen used to prevent graft rejection. Application of stem cell therapy in experimental animal models was shown to reverse cardiac remodeling, attenuate cardiac fibrosis, improve heart functions, and stimulate angiogenesis. The efficacy of stem cell therapy can be amplified by low-level laser radiation...
July 6, 2017: Lasers in Medical Science
https://www.readbyqxmd.com/read/28671086/deficiency-of-interfibrillar-mitochondria-in-post-acute-myocardial-infarction-heart-failure
#14
Yanting Geng, Yuanhui Hu, Huan Wang, Shuai Shi, Jingjing Shi, Zhiling Qiu
Mitochondrial dysfunction plays an important role in the progress of heart failure (HF). A pronounced variability of defects in mitochondrial subpopulations is reported to occur in various disease models. The aim of the study was to define the defects in the ultra structure and bioenergetic function of cardiac mitochondria in acute myocardial infarction-induced HF. AMI-induced HF rats were treated with saline (4.0ml/kg) for 8weeks. The ultra structure of myocardial mitochondrial subpopulations was assessed by electron microscope...
May 2017: Pakistan Journal of Pharmaceutical Sciences
https://www.readbyqxmd.com/read/28669047/melatonin-protected-cardiac-microvascular-endothelial-cells-against-oxidative-stress-injury-via-suppression-of-ip3r-ca-2-c-vdac-ca-2-m-axis-by-activation-of-mapk-erk-signaling-pathway
#15
Hang Zhu, Qinhua Jin, Yang Li, Qiang Ma, Jing Wang, Dandan Li, Hao Zhou, Yundai Chen
The cardiac microvascular reperfusion injury is characterized by the microvascular endothelial cells (CMECs) oxidative damage which is responsible for the progression of cardiac dysfunction. However, few strategies are available to reverse such pathologies. This study aimed to explore the mechanism by which oxidative stress induced CMECs death and the beneficial actions of melatonin on CMECs survival, with a special focused on IP3R-[Ca(2+)]c/VDAC-[Ca(2+)]m damage axis and the MAPK/ERK survival signaling. We found that oxidative stress induced by H2O2 significantly activated cAMP response element binding protein (CREB) that enhanced IP3R and VDAC transcription and expression, leading to [Ca(2+)]c and [Ca(2+)]m overload...
July 1, 2017: Cell Stress & Chaperones
https://www.readbyqxmd.com/read/28668597/mechano-sensitivity-of-mitochondrial-function-in-mouse-cardiac-myocytes
#16
REVIEW
Gentaro Iribe, Keiko Kaihara, Yohei Yamaguchi, Michio Nakaya, Ryuji Inoue, Keiji Naruse
Mitochondria are an important source of reactive oxygen species (ROS). Although it has been reported that myocardial stretch increases cellular ROS production by activating nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2), referred to as X-ROS signalling, the involvement of mitochondria in X-ROS is not clear. Mitochondria are organelles that generate adenosine triphosphate (ATP) for cellular energy needs, which are mechanical-load-dependent. Therefore, it would not be surprising if these organelles had mechano-sensitive functions associated with stretch-induced ROS production...
June 28, 2017: Progress in Biophysics and Molecular Biology
https://www.readbyqxmd.com/read/28645478/a-tspo-ligand-prevents-mitochondrial-sterol-accumulation-and-dysfunction-during-myocardial-ischemia-reperfusion-in-hypercholesterolemic-rats
#17
Julien Musman, Stéphanie Paradis, Mathieu Panel, Sandrine Pons, Caroline Barau, Claudio Caccia, Valerio Leoni, Bijan Ghaleh, Didier Morin
A major cause of cell death during myocardial ischemia-reperfusion is mitochondrial dysfunction. We previously showed that the reperfusion of an ischemic myocardium was associated with an accumulation of cholesterol into mitochondria and a concomitant strong generation of auto-oxidized oxysterols. The inhibition of mitochondrial accumulation of cholesterol abolished the formation of oxysterols and prevented mitochondrial injury at reperfusion. The aim of this study was to investigate the impact of hypercholesterolemia on sterol and oxysterol accumulation in rat cardiac cytosols and mitochondria and to analyse the effect of the translocator protein ligand 4'-chlorodiazepam on this accumulation and mitochondrial function...
June 20, 2017: Biochemical Pharmacology
https://www.readbyqxmd.com/read/28642043/mitochondrial-cx43-an-important-component-of-cardiac-preconditioning
#18
REVIEW
Antonio Rodríguez-Sinovas, Marisol Ruiz-Meana, Amanda Denuc, David García-Dorado
Connexin 43 (Cx43) forms gap junction channels that are essential for the propagation of electrical depolarization in cardiomyocytes, but also with important roles in the pathophysiology of reperfusion injury. However, more recent studies have shown that Cx43 has also important functions independent from intercellular communication between adjacent cardiomyocytes. Some of these actions have been related to the presence of Cx43 in the mitochondria of these cells (mitoCx43). The functions of mitoCx43 have not been completely elucidated, but there is strong evidence indicating that mitoCx43 modulates mitochondrial respiration at respiratory complex I, production of radical oxygen species and ATP synthesis...
June 20, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28640448/overview-of-the-muscle-cytoskeleton
#19
Christine A Henderson, Christopher G Gomez, Stefanie M Novak, Lei Mi-Mi, Carol C Gregorio
Cardiac and skeletal striated muscles are intricately designed machines responsible for muscle contraction. Coordination of the basic contractile unit, the sarcomere, and the complex cytoskeletal networks are critical for contractile activity. The sarcomere is comprised of precisely organized individual filament systems that include thin (actin), thick (myosin), titin, and nebulin. Connecting the sarcomere to other organelles (e.g., mitochondria and nucleus) and serving as the scaffold to maintain cellular integrity are the intermediate filaments...
June 18, 2017: Comprehensive Physiology
https://www.readbyqxmd.com/read/28637784/tnfr2-stimulation-promotes-mitochondrial-fusion-via-stat3-and-nf-kb-dependent-activation-of-opa1-expression
#20
Jinliang Nan, Hengxun Hu, Yong Sun, Lianlian Zhu, Yingchao Wang, Zhiwei Zhong, Jing Zhao, Na Zhang, Ya Wang, Yaping Wang, Jian Ye, Ling Zhang, Xinyang Hu, Wei Zhu, Jian'an Wang
Rationale: Mitochondria are important cellular organelles and play essential roles in maintaining cell structure and function. Emerging evidence indicates that in addition to having pro-inflammatory and pro-apoptotic effects, tumor necrosis factor α (TNFα) can, under certain circumstances, promote improvements in mitochondrial integrity and function, phenomena that can be ascribed to the existence of TNFα receptor 2 (TNFR2). Objective: The present study aimed to investigate whether and how TNFR2 activation mediates the effects of TNFα on mitochondria...
June 21, 2017: Circulation Research
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