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Cardiomyocytes and mitochondria

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https://www.readbyqxmd.com/read/30315806/hdac6-inhibition-protects-cardiomyocytes-against-doxorubicin-induced-acute-damage-by-improving-%C3%AE-tubulin-acetylation
#1
Rui Song, Yurong Yang, Han Lei, Guangxue Wang, Yong Huang, Wenlong Xue, Yinfang Wang, Lingling Yao, Yichun Zhu
Doxorubicin (Dox) is an efficacious antineoplastic drug but is limited used for its cardiotoxicity. Histone Deacetylase 6 (HDAC6) has been indicated to participate in cardiomyopathies, however, its role in Dox-induced cardiac injury is largely unknown. In this study, we firstly aimed to determine the role of HDAC6 in Dox-induced cardiomyopathy. Immunoblotting revealed that Dox increased HDAC6 protein level and activity and decreased α-tubulin acetylation level in vitro and vivo. HDAC6 knockout (HDAC6-/- ) mice showed obvious anti-Dox cardiotoxicity by conserved cardiac function monitored by echocardiography and the protection was reversed by Nocodazole, one drug lowering α-tubulin acetylation...
October 10, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/30311946/the-inner-mitochondrial-membrane-protein-ant1-modulates-il-6-expression-via-the-jnk-pathway-in-macrophages
#2
Kazuki Nakahara, Tatsuhide Tanaka, Hiroaki Okuda, Ayami Isonishi, Shoko Morita-Takemura, Kouko Tatsumi, Akio Wanaka
Mitochondria are increasingly associated with inflammation. Here, we focus on the relationship between inflammation and adenine nucleotide translocator type 1 (ANT1), which is localized in the mitochondrial inner membrane. ANT1 plays an important role in oxidative phosphorylation, and mutations in the ANT1 gene are responsible for mitochondrial diseases. Ample studies have demonstrated that ANT1 has a critical role in cardiomyocytes and neurons, but little has been reported on its functions in immune cells...
October 12, 2018: FEBS Letters
https://www.readbyqxmd.com/read/30311029/cox6b1-relieves-hypoxia-reoxygenation-injury-of-neonatal-rat-cardiomyocytes-by-regulating-mitochondrial-function
#3
Wei Zhang, Yu Wang, Junzhe Wan, Pengbo Zhang, Fei Pei
OBJECTIVE: Mitochondrial dysfunction plays a pivotal role in various pathophysiological processes of heart. Cytochrome oxidase subunit 6B1 (COX6B1) is a subunit of cytochrome oxidase. METHODS: Cardiomyocytes were isolated from neonatal SD rats (within 24 h of birth) by repeating digestion of collagenase and trypsin. COX6B1 over-expression and hypoxia/reoxygenation was conducted on neonatal rat cardiomyocytes. Cell viability, apoptosis rates, mitochondria membrane potential and mitochondrial permeabilization transition pores (mPTPs) were then determined respectively by Cell performing Counting Kit-8 (CCK-8), Annexin-V/PI assay, JC-1 assay, mPTP assay...
October 11, 2018: Biotechnology Letters
https://www.readbyqxmd.com/read/30309019/cellular-and-molecular-mechanisms-of-recessive-hereditary-methaemoglobinaemia-type-ii
#4
REVIEW
Emilio Siendones, Manuel Ballesteros, Plácido Navas
Cytochrome b5 reductase 3 (CYB5R3) is a membrane-bound NADH-dependent redox enzyme anchored to the mitochondrial outer membrane, endoplasmic reticulum, and plasma membrane. Recessive hereditary methaemoglobinaemia (RHM) type II is caused by CYB5R3 deficiency and is an incurable disease characterized by severe encephalopathy with mental retardation, microcephaly, generalized dystonia, and movement disorders. Currently, the etiology of type II RHM is poorly understood and there is no treatment for encephalopathy associated with this disease...
October 10, 2018: Journal of Clinical Medicine
https://www.readbyqxmd.com/read/30302911/mitochondrial-deformation-during-the-cardiac-mechanical-cycle
#5
E A Rog-Zielinska, E T O'toole, A Hoenger, P Kohl
Cardiomyocytes both cause and experience continual cyclic deformation. The exact effects of this deformation on the properties of intracellular organelles are not well characterized, although they are likely to be relevant for cardiomyocyte responses to active and passive changes in their mechanical environment. In the present study we provide three-dimensional ultrastructural evidence for mechanically induced mitochondrial deformation in rabbit ventricular cardiomyocytes over a range of sarcomere lengths representing myocardial tissue stretch, an unloaded "slack" state, and contracture...
October 10, 2018: Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology
https://www.readbyqxmd.com/read/30297109/cyclic-stretch-increases-mitochondrial-biogenesis-in-a-cardiac-cell-line
#6
Hyoung Kyu Kim, Yun Gyeong Kang, Seung Hun Jeong, Nammi Park, Jubert Marquez, Kyung Soo Ko, Byoung Doo Rhee, Jung-Woog Shin, Jin Han
Unlike stable and immobile cell line conditions, animal hearts contract and relax to pump blood throughout the body. Mitochondria play an essential role by producing biological energy molecules to maintain heart function. In this study, we assessed the effect of heart mimetic cyclic stretch on mitochondria in a cardiac cell line. To mimic the geometric and biomechanical conditions surrounding cells in vivo, cyclic stretching was performed on HL-1 murine cardiomyocytes seeded onto an elastic micropatterned substrate (10% elongation, 0...
October 5, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/30296408/epigenetic-upregulation-of-mir-126-induced-by-heat-stress-contributes-to-apoptosis-of-rat-cardiomyocytes-by-promoting-tomm40-transcription
#7
Xinxing Wang, Shang Wang, Weili Liu, Tianhui Wang, Jing Wang, Xiujie Gao, Ruifeng Duan, Yingying Li, Lingling Pu, Bingnan Deng, Zhaoli Chen
TOMM40 is the channel-forming subunit of a translocase of the mitochondrial outer membrane (TOM) that is essential for protein transport into mitochondria. TOMM40 plays an important role in maintaining normal mitochondrial function. The correlation between occupational thermal exposure and mitochondria dysfunction has been demonstrated; however, nothing is known about the alteration and role of TOMM40 in response to environmental heat stress. In the present study, we showed that environmental thermal exposure upregulated microRNA miR-126, consequently reducing AU-rich element RNA-binding protein 1 (AUF1)-mediated SP1 mRNA degradation and increasing TOMM40 transcription, which in turn decreased the mitochondria membrane potential and apoptosis of cardiomyocytes...
October 5, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/30290272/multiple-recycling-routes-canonical-vs-non-canonical-mitophagy-in-the-heart
#8
REVIEW
Alexandra Moyzis, Åsa B Gustafsson
The heart is composed of cardiomyocytes that require large amounts of energy to sustain contraction. Mitochondria are distinctive organelles of bacterial origin that generate most of the energy for the heart via oxidative phosphorylation. To ensure a healthy population of mitochondria that efficiently produce ATP, myocytes quickly eliminate any unhealthy or unwanted mitochondria via a process known as mitochondrial autophagy, or mitophagy. It is especially important to selectively remove damaged or aged mitochondria since they can become excessive producers of reactive oxygen species and release pro-death proteins...
October 2, 2018: Biochimica et biophysica acta. Molecular basis of disease
https://www.readbyqxmd.com/read/30284816/quadrupole-orbitrap-mass-spectrometer-based-metabonomic-elucidation-of-influences-of-short-term-di-2-ethylhexyl-phthalate-exposure-on-cardiac-metabolism-in-male-mice
#9
Wentao Li, Wenpeng Zhang, Mengyang Chang, Juan Ren, Xiaomei Zhuang, Zhenqing Zhang, Yuan Cui, Huiming Chen, Baoliang Xu, Naining Song, Haishan Li, Guolin Shen
Di(2-ethylhexyl) phthalate (DEHP) can cause severe environmental pollution. Effects of DEHP on cardiac metabolism have been reported, but its mechanism(s) of action are not fully clear. Here, we used high-resolution mass spectrometry for metabonomics and molecular biological methods to identify the different endogenous metabolites affected by DEHP that might cause changes in cardiac metabolism in mice, map the network of metabolic pathways, and reveal (at the molecular level) how DEHP affects cardiac metabolism...
October 4, 2018: Chemical Research in Toxicology
https://www.readbyqxmd.com/read/30279829/mitochondrial-deformity-confined-to-a-single-cardiomyocyte-in-human-endomyocardial-biopsy-specimens-report-of-4-cases
#10
Genzou Takemura, Hiromitsu Kanamori, Hideshi Okada, Akiko Tsujimoto, Nagisa Miyazaki, Shusaku Miyata, Hideaki Ohta, Yoshiaki Kawase, Makoto Ono, Mamoru Mochizuki, Shigeki Kobayashi, Kenji Onoue, Tomoya Nakano, Yasuhiro Sakaguchi, Hitoshi Matsuo, Masafumi Yano, Yoshihiko Saito
During electron microscopic examination of 156 consecutive human endomyocardial biopsy specimens, we found marked mitochondrial deformity within a single cardiomyocyte in each of 4 specimens. The deformed mitochondria were unevenly distributed, but the deformities were confined to the one cardiomyocyte. Those affected cardiomyocytes were accompanied by nonspecific degenerative changes such as nuclear hypertrophy and/or rarefaction of the myofibrils. Mitochondria in all other cells within the specimens appeared normal...
November 2017: Journal of Cardiology Cases
https://www.readbyqxmd.com/read/30274832/bioenergetic-feedback-between-heart-cell-contractile-machinery-and-mitochondrial-3d-deformations
#11
David Kamoun, Joachim Behar, Joseph M Leichner, Yael Yaniv
In the heart, mitochondria are arranged in pairs sandwiched between the contractile machinery, which is the major ATP consumer. Thus, in response to the contraction-relaxation cycle of the cell, the mitochondrial membrane should deform accordingly. Membrane deformations in isolated ATP synthesis or in isolated mitochondria affect ATP production. However, it is unknown whether physiological deformation of the mitochondrial membrane in response to the contraction-relaxation cycle can act as a bioenergetic signaling mechanism between ATP demand to supply...
September 6, 2018: Biophysical Journal
https://www.readbyqxmd.com/read/30273351/beta-adrenergic-activation-induces-cardiac-collapse-by-aggravating-cardiomyocyte-contractile-dysfunction-in-bupivacaine-intoxication
#12
Jun Li, Ran Duan, Yingying Zhang, Xin Zhao, Yanxin Cheng, Yongxue Chen, Jinge Yuan, Hong Li, Jianping Zhang, Li Chu, Dengyun Xia, Senming Zhao
In order to determine the role of the adrenergic system in bupivacaine-induced cardiotoxicity, a series of experiments were performed. In an animal experiment, male Sprague-Dawley (SD) rats under chloral hydrate anesthesia received intravenous bupivacaine, followed by an intravenous injection of adrenalin or isoprenalin, and the electrocardiogram (ECG), left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), the maximum rate of rise of left ventricular pressure (+dP/dtmax) and the maximum rate of pressure decrease (-dP/dtmax) were continually monitored...
2018: PloS One
https://www.readbyqxmd.com/read/30251118/leptin-induced-cardiomyocyte-hypertrophy-is-associated-with-enhanced-mitochondrial-fission
#13
Chian Ju Jong, Justin Yeung, Emily Tseung, Morris Karmazyn
Cardiac pathology including hypertrophy has been associated with an imbalance between mitochondrial fission and fusion. Generally, well-balanced mitochondrial fission and fusion are essential for proper functions of mitochondria. Leptin is a 16-kDa appetite-suppressing protein which has been shown to induce cardiomyocyte hypertrophy. In the present study, we determined whether leptin can influence mitochondrial fission or fusion and whether this can be related to its hypertrophic effect. Cardiomyocytes treated for 24 h with 3...
September 24, 2018: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/30248666/cardiac-shock-wave-therapy-attenuates-cardiomyocyte-apoptosis-after-acute-myocardial-infarction-in-rats
#14
Yunhe Zhang, Tao Shen, Bing Liu, Dapeng Dai, Jianping Cai, Cong Zhao, Ling Du, Na Jia, Qing He
BACKGROUND/AIMS: Researches have showed that cardiac shock wave therapy (CSWT) could improve left ventricular function and attenuate LV remodeling of the ischemic heart. Apoptosis plays an important role in myocardial infarction and determines heart function and prognosis. However, it is still not clear whether CSWT is sufficient to attenuate acute myocardial infarction (AMI) induced cardiomyocyte apoptosis in vivo. In this study, we used a rat model to examine whether CSWT could attenuate cardiomyocyte apoptosis after AMI and to explore potential mechanisms...
2018: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/30246714/effect-of-the-shensong-yangxin-capsule-on-energy-metabolism-in-angiotensin-ii-induced-cardiac-hypertrophy
#15
Bei-Lei Liu, Mian Cheng, Shan Hu, Shun Wang, Le Wang, Zheng-Qing Hu, Cong-Xin Huang, Hong Jiang, Gang Wu
Background: Shensong Yangxin Capsule (SSYX), traditional Chinese medicine, has been used to treat arrhythmias, angina, cardiac remodeling, cardiac fibrosis, and so on, but its effect on cardiac energy metabolism is still not clear. The objective of this study was to investigate the effects of SSYX on myocardium energy metabolism in angiotensin (Ang) II-induced cardiac hypertrophy. Methods: We used 2 μl (10-6 mol/L) AngII to treat neonatal rat cardiomyocytes (NRCMs) for 48 h...
October 5, 2018: Chinese Medical Journal
https://www.readbyqxmd.com/read/30242115/the-creatine-kinase-system-as-a-therapeutic-target-for-myocardial-ischaemia-reperfusion-injury
#16
REVIEW
Fang Cao, Sevasti Zervou, Craig A Lygate
Restoring blood flow following an acute myocardial infarction saves lives, but results in tissue damage due to ischaemia-reperfusion injury (I/R). Ameliorating this damage is a major research goal to improve recovery and reduce subsequent morbidity due to heart failure. Both the ischaemic and reperfusion phases represent crises of cellular energy provision in which the mitochondria play a central role. This mini-review will explore the rationale and therapeutic potential of augmenting the creatine kinase (CK) energy shuttle, which constitutes the primary short-term energy buffer and transport system in the cardiomyocyte...
September 20, 2018: Biochemical Society Transactions
https://www.readbyqxmd.com/read/30239560/lncrna-hotair-inhibition-aggravates-oxidative-stress-induced-h9c2-cells-injury-through-suppression-of-mmp2-by-mir-125
#17
Linlin Li, Mengna Zhang, Weizhen Chen, Ruirui Wang, Zi Ye, Yanyan Wang, Xiao Li, Cheguo Cai
Acute myocardial infarction (AMI) is one of the major causes of morbidity and mortality in the world. Ischemia/reperfusion (I/R) injury-induced cardiomyocytes death is the main obstacle that limits the heart function recovery of the AMI patients. Reactive oxygen species (ROS) generated by mitochondria is the main pathological stimulus of cardiomyocytes death during heart I/R injury process. Hence, to understand the underlying mechanism of cardioymocytes proliferation and apoptosis under oxidative stress is crucial for effective AMI therapy...
October 1, 2018: Acta Biochimica et Biophysica Sinica
https://www.readbyqxmd.com/read/30236513/loss-of-thioredoxin-2-alters-mitochondrial-respiratory-function-and-induces-cardiomyocyte-hypertrophy
#18
Chunyan Hu, Hao Zhang, Zhengdong Qiao, Yueqian Wang, Peng Zhang, Dan Yang
Thioredoxin 2 (Trx2), as a member of the thioredoxin system in mitochondria, is involved in controlling mitochondrial redox state. However, the role of Trx2 in cardiac biology is not fully understood. In the present study, the expression of Trx2 is silenced in quiescent neonatal rat ventricular cardiomyocytes (NRVCs) and mitochondrial respiratory function and cardiomyocyte hypertrophy are assessed. The results show that Trx2 depletion does not induce significant cytotoxicity in quiescent NRVCs. Remarkably, Trx2 depletion results in cardiomyocyte hypertrophy as determined by increased cell size and protein synthesis...
November 1, 2018: Experimental Cell Research
https://www.readbyqxmd.com/read/30231960/real-time-microwave-exposure-induces-calcium-efflux-in-primary-hippocampal-neurons-and-primary-cardiomyocytes
#19
Hui Wang, Jing Zhang, Shao Hua Hu, Sheng Zhi Tan, Bo Zhang, Hong Mei Zhou, Rui Yun Peng
OBJECTIVE: To detect the effects of microwave on calcium levels in primary hippocampal neurons and primary cardiomyocytes by the real-time microwave exposure combined with laser scanning confocal microscopy. METHODS: The primary hippocampal neurons and primary cardiomyocytes were cultured and labeled with probes, including Fluo-4 AM, Mag-Fluo-AM, and Rhod-2, to reflect the levels of whole calcium [Ca2+], endoplasmic reticulum calcium [Ca2+]ER, and mitochondrial calcium [Ca2+]MIT, respectively...
August 2018: Biomedical and Environmental Sciences: BES
https://www.readbyqxmd.com/read/30224925/sykt-alleviates-doxorubicin-induced-cardiotoxicity-via-modulating-ros-mediated-p53-and-mapk-signal-pathways
#20
Ting Chen, Zhiyong Deng, Ruilian Zhao, Hongmei Shen, Wenhui Li
Backgrounds. Doxorubicin (DOX) is an effective therapeutic drug for malignant tumors; however, its clinical applications were limited by its side effects, especially the cardiotoxicity caused by ROS-mediated p53 and MAPK signal pathways' activation-induced cell apoptosis. Sanyang Xuedai mixture (SYKT) has been reported as an antioxidant agent and attenuated DOX-induced cardiotoxicity by targeting ROS-mediated apoptosis, but the mechanisms are still not fully delineated. Objective. This study aimed at investigating whether SYKT alleviated DOX-induced cardiotoxicity by inhibiting ROS-mediated apoptosis and elucidating the role of ROS-mediated p53 and MAPK signal pathways' activation in this process...
2018: Evidence-based Complementary and Alternative Medicine: ECAM
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