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Cardiomyocytes and mitochondria

Chih-Yang Huang, Chao-Hung Lai, Chia-Hua Kuo, Shu-Fen Chiang, Pei-Ying Pai, Jing-Ying Lin, Chih-Fen Chang, Vijaya Padma Viswanadha, Wei-Wen Kuo, Chih-Yang Huang
Mitochondrial dysfunction is a major contributor to myocyte loss and the development of heart failure. Myocytes have quality control mechanisms to retain functional mitochondria by removing damaged mitochondria via specialized autophagy, i.e., mitophagy. The underlying mechanisms of fission affect the survival of cardiomyocytes, and left ventricular function in the heart is poorly understood. Here, we demonstrated the direct effect and potential mechanisms of mitochondrial functional defects associated with abnormal mitochondrial dynamics in heart failure...
August 9, 2018: Journal of Molecular and Cellular Cardiology
Yao-Chih Yang, Cheng-Yen Tsai, Chien-Lin Chen, Chia-Hua Kuo, Chien-Wen Hou, Shi-Yann Cheng, Ritu Aneja, Chih-Yang Huang, Wei-Wen Kuo
Diabetic patients exhibit serum AGE accumulation, which is associated with reactive oxygen species (ROS) production and diabetic cardiomyopathy. ROS-induced PKCδ activation is linked to mitochondrial dysfunction in human cells. However, the role of PKCδ in cardiac and mitochondrial dysfunction caused by AGE in diabetes is still unclear. AGE-BSA-treated cardiac cells showed dose- and time-dependent cell apoptosis, ROS generation, and selective PKCδ activation, which were reversed by NAC and rotenone. Similar tendency was also observed in diabetic and obese animal hearts...
August 2018: Aging and Disease
Alexandre Prola, Zuzana Nichtova, Julie Pires Da Silva, Jérôme Piquereau, Kevin Monceaux, Arnaud Guilbert, Mélanie Gressette, Renée Ventura-Clapier, Anne Garnier, Ivan Zahradnik, Marta Novotova, Christophe Lemaire
AIMS: Endoplasmic reticulum (ER) stress has recently emerged as an important mechanism involved in the pathogenesis of cardiovascular diseases. However, the molecular mechanisms by which ER stress leads to cardiac dysfunction remain poorly understood. METHODS AND RESULTS: In the present study, we evaluated the early cardiac effects of ER stress induced by tunicamycin (TN) in mice. Echocardiographic analysis indicated that TN-induced ER stress led to a significant impairment of the cardiac function...
August 3, 2018: Cardiovascular Research
Celal Guven
Cardiac hypertrophy is associated with mitochondrial dysfunctions, which leads to heart failure if sustained. The aim of present study is to test hypothesis whether activation of mitochondrial KATP channel (mitoKATP) by diazoxide improve mitochondrial membrane potential (MMP) and oxidative stress in an in vitro model of cardiac hypertrophy. Rat cardiomyocytes cell line (H9c2) was used to create four groups as control, diazoxide, hypertrophy, hypertrophy and diazoxide. Norepinephrine was used to induce hypertrophy...
July 30, 2018: Cellular and Molecular Biology
Jieying Peng, Yuhao Zhou, Zhiyu Zhang, Zhiming Wang, Lingtong Gao, Xiao Zhang, Zhou Fang, Guangyao Li, Huaiyan Chen, Hongxing Yang, Lu Gao
The intra-uterine and external environmental factors not only affect the early development of fetuses, their interaction with genesis will also substantially program the physiological functions of offspring throughout life. Synthetic glucocorticoid (GC) is widely used for the management of women at risk of preterm birth or undergone autoimmune diseases. However, excess GC might cause a number of chronic diseases in later life. In the present study, we set up a programming rat model by daily injection of dexamethasone (DEX) since 14...
August 6, 2018: Cell Death & Disease
Rita Ferreira, Rita Nogueira-Ferreira, Fábio Trindade, Rui Vitorino, Scott K Powers, Daniel Moreira-Gonçalves
Mammals respond to muscular exercise by increasing cardiac output to meet the increased demand for oxygen in the working muscles and it is well-established that regular bouts of exercise results in myocardial remodeling. Depending on exercise type, intensity and duration, these cardiac adaptations lead to changes in the energetic substrates required to sustain cardiac contractility. In contrast to the failing heart, fatty acids are the preferred substrate in the trained heart, though glucose metabolism is also enhanced to support oxidative phosphorylation...
August 2, 2018: Metabolism: Clinical and Experimental
Shanjie Wang, Zhijing Zhao, Xinyu Feng, Zheng Cheng, Zhenyu Xiong, Tingting Wang, Jie Lin, Mingming Zhang, Jianqiang Hu, Yanhong Fan, Russel J Reiter, Haichang Wang, Dongdong Sun
Mitophagy eliminates dysfunctional mitochondria and thus plays a cardinal role in diabetic cardiomyopathy (DCM). We observed the favourable effects of melatonin on cardiomyocyte mitophagy in mice with DCM and elucidated their underlying mechanisms. Electron microscopy and flow cytometric analysis revealed that melatonin reduced the number of impaired mitochondria in the diabetic heart. Other than decreasing mitochondrial biogenesis, melatonin increased the clearance of dysfunctional mitochondria in mice with DCM...
July 31, 2018: Journal of Cellular and Molecular Medicine
Huan He, Yong Luo, Yang Qiao, Zeyu Zhang, Dong Yin, Jianguo Yao, Jiegen You, Ming He
Doxorubicin (Dox) induces cardiotoxicity, thereby limiting its clinical application for chemotherapy of cancer. The mechanism of cardiotoxicity includes the production of excess intracellular ROS. 14-3-3s have been found to protect the myocardium against various types of injury. Curcumin (Cur) is a polyphenolic compound that is derived from turmeric and has multiple bioactivities, including anti-oxidative and radical-scavenging activities that exert cytoprotection. We hypothesize that the cardioprotective effects of Cur are exerted by regulating 14-3-3γ...
July 31, 2018: Food & Function
Guihao Chen, Yuejin Yang, Chuansheng Xu, Shuo Gao
Timely and efficient reperfusion of the occluded coronary artery is the best strategy for decreasing myocardial infarct size in patients with a ST-segment elevated myocardial infarction. However, reperfusion per se can result in further cardiomyocyte death, a phenomenon known as reperfusion injury. The opening of the mitochondrial permeability transition pore (mPTP), with the decrease of the mitochondrial membrane potential (MMP), or mitochondrial depolarization, is universally recognized as the final step of reperfusion injury and is responsible for mitochondrial and cardiomyocyte death...
July 13, 2018: Journal of Visualized Experiments: JoVE
Majid Khaksar, Mansour Sayyari, Jafar Rezaie, Ayda Pouyafar, Soheila Montazersaheb, Reza Rahbarghazi
Murine c-kit+ cardiac cells were isolated and enriched by magnetic activated cell sorting technique. c-kit+ cells viability and colony-forming activity were evaluated by MTT and clonogenic assay. c-kit+ cells were exposed to endothelial, pericyte, and cardiomyocyte induction media containing 30mM glucose for 7 days. We monitored the level of endothelial (VE-cadherin, CD31, and vWF), pericyte (NG2 , α-SMA, and PDGFR-β), and cardiomyocyte markers (cTnT) using flow cytometry, real-time Polymerase Chain Reaction (PCR), and Enzyme-Linked Immunosorbent Assay (ELISA) analyses...
July 26, 2018: Cell Biochemistry and Function
Zeyu Zhang, Huan He, Yang Qiao, Jiyi Huang, Zelong Wu, Ping Xu, Dong Yin, Ming He
Tanshinone IIA is an important component that is isolated from danshen ( Salvia miltiorrhiza ), which is known to be beneficial for cardiovascular health. In this study, we determined the effects of Tanshinone IIA and its underlying mechanisms of action in an anoxia/reoxygenation (A/R) cell line model. Prior to inducing A/R injury, rat cardiomyocyte-derived cell line H9c2 was stimulated with 8  μ M of Tanshinone IIA for 48 hours. When compared with the A/R group, the Tanshinone IIA treatment significantly increased cell viability and decreased lactate dehydrogenase activity...
2018: Oxidative Medicine and Cellular Longevity
Bangwei Wu, Jian Li, Huanchun Ni, Xinyu Zhuang, Zhiyong Qi, Qiying Chen, Zhichao Wen, Haiming Shi, Xinping Luo, Bo Jin
Mitochondrial dynamic imbalance associates with several cardiovascular diseases. However, the role of mitochondrial dynamics in TLR4 activation-mediated dilated cardiomyopathy (DCM) progress remains unknown. A model of experimental autoimmune myocarditis (EAM) was established in BALB/c mice on which TLR4 activation by LPS-EB or TLR4 inhibition by LPS-RS was performed to induce chronic inflammation for 5 weeks. TLR4 activation promoted the transition of EAM to DCM as demonstrated by increased cardiomyocyte apoptosis, myocardial fibrosis, ventricular dilatation, and declined heart function...
2018: Oxidative Medicine and Cellular Longevity
Laura Rinaldi, Sofya Pozdniakova, Vignesh Jayarajan, Christian Troidl, Yaser Abdallah, Muhammad Aslam, Yury Ladilov
AIMS: Disturbance of mitochondrial function significantly contributes to the myocardial injury that occurs during reperfusion. Increasing evidence suggests a role of intra-mitochondrial cyclic AMP (cAMP) signaling in promoting respiration and ATP synthesis. Mitochondrial levels of cAMP are controlled by type 10 soluble adenylyl cyclase (sAC) and phosphodiesterase 2 (PDE2), however their role in the reperfusion-induced injury remains unknown. Here we aimed to examine whether sAC may support cardiomyocyte survival during reperfusion...
July 22, 2018: Biochimica et Biophysica Acta
Rômulo D Novaes, Viviane G S Mouro, Reggiani V Gonçalves, Andrea A S Mendonça, Eliziária C Santos, Maria C Q Fialho, Mariana Machado-Neves
Large amounts of aluminum (Al) are found in wastewater from industrial bauxite mining, which is often responsible for the contamination of drinking water sources in urban and rural communities. Although this metal exhibits broad environmental distribution, its cardiac repercussions are poorly understood, making it difficult to establish diagnostic criteria in cases of Al intoxication. In the absence of clinical data, we used a preclinical model to investigate the impact of Al exposure on heart bioaccumulation, molecular oxidation, micromineral distribution, structural and ultrastructural remodeling of the cardiac tissue...
July 17, 2018: Environmental Pollution
Xibo Jing, Jingxiao Yang, Lu Jiang, Jianghong Chen, Haiyan Wang
BACKGROUND/AIMS: Myocardial apoptosis plays an important role in doxorubicin (Dox) cardiotoxicity. MicroRNA-29 (miR-29) is suggested to function as an anti-fibrotic factor with potential therapeutic effects on cardiac fibrosis. However, it has not been shown whether there is an association between miR-29b and myocardial apoptosis. METHODS: Male Wistar rats were transfected with miR-29b agomir by local delivery to the myocardium prior to Dox treatment. Rat cardiomyocytes were pretreated with miR-29b mimics or inhibitor followed by Dox incubation in vitro...
July 19, 2018: Cellular Physiology and Biochemistry
Hirokazu Tsubone, Tatsushi Mutoh
We studied the effect of glucose supply on mitochondrial respiratory function (MRF) of neonatal rat cardiomyocytes, using a novel extracellular flux analysis. Fundamental respiratory parameters regarding oxygen consumption rate in mitochondria showed glucose concentration-dependent changes, where a significant increase or decrease in these parameters was observed to be associated with glucose concentrations ranging between 10% and 1,000% of the concentration used in standard medium (3,151 mg/L), respectively...
July 19, 2018: Clinical and Experimental Pharmacology & Physiology
Yue Xi, Wenwen Wang, Li Wang, Ji Pan, Yisen Cheng, Feihai Shen, Zhiying Huang
Triptolide (TP), a major active component of Tripterygium wilfordii Hook f., is widely used in the treatment of inflammation and autoimmune disorders. Its clinical application is limited by severe adverse effects, especially cardiotoxicity. Accumulative evidences indicate that TP induces DNA damage by inhibiting RNA polymerase. Considering the relationship among DNA damage, p53, and the role of p53 in mitochondria-dependent apoptosis, we speculate that TP-induced cardiotoxicity results from p53 activation. In this study, the role of p53 in TP-induced cardiotoxicity was investigated in H9c2 cells, primary cardiomyocytes, and C57BL/6 genetic background p53-/- mice...
July 18, 2018: Toxicology and Applied Pharmacology
Jordan M Johnson, Patrick J Ferrara, Anthony R P Verkerke, Chanel B Coleman, Edward J Wentzler, P Darrell Neufer, Kimberly A Kew, Lisandra E de Castro Brás, Katsuhiko Funai
Barth Syndrome (BTHS) is an X-linked recessive disorder characterized by cardiomyopathy and muscle weakness. The underlying cause of BTHS is a mutation in the tafazzin (TAZ) gene, a key enzyme of cardiolipin biosynthesis. The lack of CL arising from loss of TAZ function results in destabilization of the electron transport system, promoting oxidative stress that is thought to contribute to development of cardioskeletal myopathy. Indeed, in vitro studies demonstrate that mitochondria-targeted antioxidants improve contractile capacity in TAZ-deficient cardiomyocytes...
July 2, 2018: Journal of Molecular and Cellular Cardiology
Nicola Manzella, Yohan Santin, Damien Maggiorani, Hélène Martini, Victorine Douin-Echinard, Joao F Passos, Frank Lezoualc'h, Claudia Binda, Angelo Parini, Jeanne Mialet-Perez
Cellular senescence, the irreversible cell cycle arrest observed in somatic cells, is an important driver of age-associated diseases. Mitochondria have been implicated in the process of senescence, primarily because they are both sources and targets of reactive oxygen species (ROS). In the heart, oxidative stress contributes to pathological cardiac ageing, but the mechanisms underlying ROS production are still not completely understood. The mitochondrial enzyme monoamine oxidase-A (MAO-A) is a relevant source of ROS in the heart through the formation of H2 O2 derived from the degradation of its main substrates, norepinephrine (NE) and serotonin...
July 12, 2018: Aging Cell
An Xie, Anyu Zhou, Hong Liu, Guangbin Shi, Man Liu, Kenneth R Boheler, Samuel C Dudley
INTRODUCTION: Ca2+ release from sarcoplasmic reticulum (SR) is known to contribute to automaticity via the cytoplasmic Na+-Ca2+ exchanger (NCX). Mitochondria participate in Ca2+ cycling. We studied the role of mitochondrial Ca2+ flux in ventricular spontaneous electrical activity. METHODS: Spontaneously contracting mouse embryonic stem cells (ESC)-derived ventricular cardiomyocytes (CMs) were differentiated from wild type and ryanodine receptor type 2 (RYR2) knockout mouse ESCs and differentiated for 19-21 days...
2018: PloS One
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