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Cardiac myocyte

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https://www.readbyqxmd.com/read/28542952/compensatory-and-decompensatory-alterations-in-cardiomyocyte-ca-2-dynamics-in-hearts-with-diastolic-dysfunction-following-aortic-banding
#1
Sara Gattoni, Åsmund Treu Røe, Jan Magnus Aronsen, Ivar Sjaastad, William E Louch, Nicolas P Smith, Steven A Niederer
KEY POINTS: At the cellular level cardiac hypertrophy causes remodelling, leading to changes in ionic channel, pump and exchanger densities and kinetics. Previous studies have focused on quantifying changes in channels, pumps and exchangers without quantitatively linking these changes with emergent cellular scale functionality. Two biophysical cardiac cell models were created, parameterized and validated and are able to simulate electrophysiology and calcium dynamics in myocytes from control sham operated rats and aortic-banded rats exhibiting diastolic dysfunction...
May 21, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/28542130/activation-of-transient-receptor-potential-vanilloid-4-involves-in-hypoxia-reoxygenation-injury-in-cardiomyocytes
#2
Qiong-Feng Wu, Cheng Qian, Ning Zhao, Qian Dong, Jing Li, Bin-Bin Wang, Lei Chen, Lixiu Yu, Bing Han, Yi-Mei Du, Yu-Hua Liao
Transient receptor potential vanilloid 4 (TRPV4) is highly expressed in heart and vessels and can be activated during myocardial ischemia/reperfusion (I/R). Recently, we found that treatment with a selective TRPV4 antagonist HC-067047 significantly reduced infarct size, decreased troponin T levels and improved cardiac function in murine model myocardial I/R. This study was undertaken to investigate the mechanism underlying TRPV4-mediated myocardial I/R injury. To mimic myocardial I/R injury, we established a hypoxia/reoxygenation (H/R) model in H9C2 cells and neonatal rat ventricle myocytes (NRVMs) in vitro...
May 25, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28539361/synthesis-of-the-ca-2-mobilizing-messengers-naadp-and-cadpr-by-intracellular-cd38-enzyme-in-mouse-heart-role-in-%C3%AE-adrenoceptor-signaling
#3
Wee K Lin, Emma L Bolton, Wilian A Cortopassi, Yanwen Wang, Fiona O'Brien, Matylda Maciejewska, Matthew P Jacobson, Clive Garnham, Margarida Ruas, John Parrington, Ming Lei, Rebecca Sitsapesan, Antony Galione, Derek A Terrar
Nicotinic acid adenine dinucleotide phosphate (NAADP) and cyclic ADP-ribose (cADPR) are Ca(2+)-mobilizing messengers important for modulating cardiac excitation-contraction coupling and pathophysiology. CD38, which belongs to the ADP-ribosyl cyclase (ARC) family, catalyzes synthesis of both NAADP and cADPR in vitro However, it remains unclear whether this is the main enzyme for their production under physiological conditions. Here, we show that membrane fractions from WT but not CD38(-/-) mouse hearts supported NAADP and cADPR synthesis...
May 24, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28536966/a-comprehensive-review-of-the-bioenergetics-of-fatty-acid-and-glucose-metabolism-in-the-healthy-and-failing-heart-in-nondiabetic-condition
#4
REVIEW
Ashish Gupta, Brian Houston
The function of the heart is defined by its ability to deliver adequate cardiac output to meet the requirements of the body both at rest and with exertion. To fill this role, the heart demonstrates an impressive capacity to tightly regulate energy generation and consumption. Energy production and transfer within cardiac myocytes primarily relies on the process of oxidative phosphorylation. In the failing heart, there is an imbalance between the work of the cardiac system and the energy required to generate this work...
May 24, 2017: Heart Failure Reviews
https://www.readbyqxmd.com/read/28536695/cardiac-protection-of-valsartan-on-juvenile-rats-with-heart-failure-by-inhibiting-activity-of-camkii-via-attenuating-phosphorylation
#5
Yao Wu, Feifei Si, Xiaojuan Ji, Kunfeng Jiang, Sijie Song, Qijian Yi
Background. This study was undertaken to determine relative contributions of phosphorylation and oxidation to the increased activity of calcium/calmodulin-stimulated protein kinase II (CaMKII) in juveniles with cardiac myocyte dysfunction due to increased pressure overload. Methods. Juvenile rats underwent abdominal aortic constriction to induce heart failure. Four weeks after surgery, rats were then randomly divided into two groups: one group given valsartan (HF + Val) and the other group given placebo (HF + PBO)...
2017: BioMed Research International
https://www.readbyqxmd.com/read/28534086/neuronal-nitric-oxide-synthase-modulation-of-intracellular-ca-2-handling-overrides-fatty-acid-potentiation-of-cardiac-inotropy-in-hypertensive-rats
#6
Chun Li Jin, Ming Zhe Yin, Jin Chul Paeng, Seunggyun Ha, Jeong Hoon Lee, Peng Jin, Chun Zi Jin, Zai Hao Zhao, Yue Wang, Keon Wook Kang, Chae Hun Leem, Jong-Wan Park, Sung Joon Kim, Yin Hua Zhang
Cardiac neuronal nitric oxide synthase (nNOS) is an important molecule that regulates intracellular Ca(2+) homeostasis and contractility of healthy and diseased hearts. Here, we examined the effects of nNOS on fatty acid (FA) regulation of left ventricular (LV) myocyte contraction in sham and angiotensin II (Ang II)-induced hypertensive (HTN) rats. Our results showed that palmitic acid (PA, 100 μM) increased the amplitudes of sarcomere shortening and intracellular ATP in sham but not in HTN despite oxygen consumption rate (OCR) was increased by PA in both groups...
May 22, 2017: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/28526910/expression-and-regulation-of-type-2a-protein-phosphatases-and-alpha4-signalling-in-cardiac-health-and-hypertrophy
#7
Olga Eleftheriadou, Andrii Boguslavskyi, Michael R Longman, Jonathan Cowan, Asvi Francois, Richard J Heads, Brian E Wadzinski, Ali Ryan, Michael J Shattock, Andrew K Snabaitis
Cardiac physiology and hypertrophy are regulated by the phosphorylation status of many proteins, which is partly controlled by a poorly defined type 2A protein phosphatase-alpha4 intracellular signalling axis. Quantitative PCR analysis revealed that mRNA levels of the type 2A catalytic subunits were differentially expressed in H9c2 cardiomyocytes (PP2ACβ > PP2ACα > PP4C > PP6C), NRVM (PP2ACβ > PP2ACα = PP4C = PP6C), and adult rat ventricular myocytes (PP2ACα > PP2ACβ > PP6C > PP4C)...
July 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28526706/cardiac-hyporesponsiveness-in-severe-sepsis-is-associated-with-nitric-oxide-dependent-activation-of-g-protein-receptor-kinase
#8
Daniela Dal-Secco, Silvia DalBó, Natalia E S Lautherbach, Fábio N Gava, Mara Rubia Nunes Celes, Patricia Oliveira Benedet, Adriana H Souza, Juliana Akinaga, Vanessa Lima, Katiussia P Silva, Luiz Ricardo A Kiguti, Marcos A Rossi, Isis do Carmo Kettelhut, André Sampaio Pupo, Fernando Queiroz Cunha, Jamil Assreuy
G protein-coupled receptor kinase isoform 2 (GRK2) has a critical role in physiological and pharmacological responses to endogenous and exogenous substances. Sepsis causes an important cardiovascular dysfunction in which nitric oxide (NO) has a relevant role. The present study aimed to assess the putative effect of inducible NO synthase (NOS-2)-derived NO on the activity of GRK2 in the context of septic cardiac dysfunction. C57BL/6 mice were submitted to severe septic injury by cecal ligation and puncture (CLP)...
May 19, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28526544/interleukin-18-gene-deletion-protects-against-sepsis-induced-cardiac-dysfunction-by-inhibiting-pp2a-activity
#9
Yoshitaka Okuhara, Shunichi Yokoe, Toshihiro Iwasaku, Akiyo Eguchi, Koichi Nishimura, Wen Li, Makiko Oboshi, Yoshiro Naito, Toshiaki Mano, Michio Asahi, Haruki Okamura, Tohru Masuyama, Shinichi Hirotani
BACKGROUND: Interleukin-18 (IL-18) neutralization protects against lipopolysaccharide (LPS)-induced injuries, including myocardial dysfunction. However, the mechanism is yet to be fully elucidated. The aim of the present study was to determine whether IL-18 gene deletion prevents sepsis-induced cardiac dysfunction and to elucidate the potential mechanisms underlying IL-18-mediated cardiotoxicity by LPS. METHODS AND RESULTS: Ten-week-old male wild-type (WT) and IL-18 knockout (IL-18 KO) mice were intraperitoneally administered LPS...
May 4, 2017: International Journal of Cardiology
https://www.readbyqxmd.com/read/28522761/ventricular-action-potential-adaptation-to-regular-exercise-role-of-%C3%AE-adrenergic-and-katp-channel-function
#10
Xinrui Wang, Robert H Fitts
Regular exercise-training is known to affect the action potential duration (APD) and improve heart function, but the involvement by β-adrenergic receptor (β-AR) subtypes and/or KATP channel is unknown. To address this, female and male Sprague-Dawley rats were randomly assigned to voluntary wheel running or control groups and after 6-8 weeks training anesthetized and myocytes isolated. Exercise-training significantly increased APD of apex and base myocytes at 1Hz, while decreasing the APD at 10Hz. Ca(2+) transient durations reflected the changes observed in APD, while Ca(2+) transient amplitudes were unaffected by wheel running...
May 18, 2017: Journal of Applied Physiology
https://www.readbyqxmd.com/read/28514938/characterization-and-standardization-of-cultured-cardiac-fibroblasts-for-ex-vivo-models-of-heart-fibrosis-and-heart-ischemia
#11
Yue Zhou, Arthur Mark Richards, Peipei Wang
A full understanding of cardiac fibroblast (cFB) biology is essential to study the adverse cardiac remodeling and recovery of myocardium infarction. However, compared to cardiac myocytes, cFB are less well-characterized. Important questions including the variability introduced by cell age (neonatal vs. adult), culture conditions (passage, plate coating and culture medium), and responses to stimuli (e.g. hypoxia and drug treatments) have not been well addressed and standardization of techniques is lacking. This variability invites inconsistency and the confounding of study conclusions...
May 17, 2017: Tissue Engineering. Part C, Methods
https://www.readbyqxmd.com/read/28512310/fgf23-fgfr4-mediated-left-ventricular-hypertrophy-is-reversible
#12
Alexander Grabner, Karla Schramm, Neerupma Silswal, Matt Hendrix, Christopher Yanucil, Brian Czaya, Saurav Singh, Myles Wolf, Sven Hermann, Jörg Stypmann, Giovana Seno Di Marco, Marcus Brand, Michael J Wacker, Christian Faul
Fibroblast growth factor (FGF) 23 is a phosphaturic hormone that directly targets cardiac myocytes via FGF receptor (FGFR) 4 thereby inducing hypertrophic myocyte growth and the development of left ventricular hypertrophy (LVH) in rodents. Serum FGF23 levels are highly elevated in patients with chronic kidney disease (CKD), and it is likely that FGF23 directly contributes to the high rates of LVH and cardiac death in CKD. It is currently unknown if the cardiac effects of FGF23 are solely pathological, or if they potentially can be reversed...
May 16, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28512107/divergent-requirements-for-ezh1-in-heart-development-versus-regeneration
#13
Shanshan Ai, Xianhong Yu, Yumei Li, Yong Peng, Chen Li, Yanzhu Yue, Ge Tao, Chuan-Yun Li, William T Pu, Aibin He
Rationale: Polycomb repressive complex 2 (PRC2) is a major epigenetic repressor that deposits methylation on histone H3 on lysine 27 (H3K27me) and controls differentiation and function of many cells, including cardiac myocytes. EZH1 and EZH2 are two alternative catalytic subunits with partial functional redundancy. The relative roles of EZH1 and EZH2 in heart development and regeneration are unknown. Objective: We compared the roles of EZH1 versus EZH2 in heart development and neonatal heart regeneration. Methods and Results: Heart development was normal in Ezh1(-/-) (E1KO) and Ezh2(f/f)::cTNT(-Cre) (E2KO) embryos...
May 16, 2017: Circulation Research
https://www.readbyqxmd.com/read/28511329/-therapeutic-effect-of-combined-use-of-fgf1-loaded-nano-liposomes-and-ultrasound-targeted-microbubble-destruction-technique-on-treating-rats-with-experimental-diabetic-cardiomyopathy
#14
M Zhang, Y Z Zhao, W C Ma, J L Xu, J L Wang, M J Chen, L Yu, Y N Chen
Objective: The therapeutic effect of acid fibroblast growth factor 1(FGF1) on rats with diabetic cardiomyopathy (DCM) was evaluated by using nano-liposomes combined with ultrasound-targeted microbubble destruction technique (UTMD). Methods: The FGF1-loaded nano-liposomes were prepared by water-in-water emulsion method combined with lyophilization technique.TypeⅠdiabetes model was induced by intraperitoneal injection of streptozotocin (STZ, 70 mg/kg) in 60 male SD rats.Sixteen weeks later, diabetic rats were randomly divided into: placebo group (saline treatment), FGF1 group, FGF1-loaded nano-liposomes group, and FGF1-loaded nano-liposomes plus UTMD group (n=15 each)...
May 24, 2017: Zhonghua Xin Xue Guan Bing za Zhi
https://www.readbyqxmd.com/read/28509708/pvcs-pvc-induced-cardiomyopathy-and-the-role-of-catheter-ablation
#15
Esseim Sharma, Karuppiah Arunachalam, Mengyang Di, Antony Chu, Abhishek Maan
Premature ventricular contractions (PVCs) are common arrhythmias noticed in the clinical setting because of premature depolarization of the ventricular myocytes. Although often thought to be reflective of underlying disease rather than intrinsically harmful, PVCs have recently been linked with worse outcomes in patients without significant cardiac disease. Long-term exposure to a high PVC burden can lead to the development of PVC-induced cardiomyopathy. The pathogenesis of this condition is poorly understood at the current time...
June 2017: Critical Pathways in Cardiology
https://www.readbyqxmd.com/read/28506553/inhibition-of-12-15-lo-ameliorates-cvb3-induced-myocarditis-by-activating-nrf2
#16
Feng Ai, Jiayong Zheng, Yanwei Zhang, Taibing Fan
Cardiac 12/15-lipoxygenase (12/15-LO) was reported to be markedly up-regulated and involved in the development of heart failure. Nuclear factor E2-related factor 2 (Nrf2) plays anti-inflammatory and anti-oxidation roles in response to oxidative stress. However, the role of 12/15-LO in viral myocarditis (VMC) and its underlying molecular mechanism have not yet been elucidated. Here, we demonstrated that 12/15-LO was up-regulated and Nrf2 was down-regulated in coxsackievirus B3 (CVB3)-infected mice and cardiac myocytes...
May 12, 2017: Chemico-biological Interactions
https://www.readbyqxmd.com/read/28504961/wnt-%C3%AE-catenin-pathway-in-arrhythmogenic-cardiomyopathy
#17
REVIEW
Alessandra Lorenzon, Martina Calore, Giulia Poloni, Leon J De Windt, Paola Braghetta, Alessandra Rampazzo
Wnt/β-catenin signaling pathway plays essential roles in heart development as well as cardiac tissue homoeostasis in adults. Abnormal regulation of this signaling pathway is linked to a variety of cardiac disease conditions, including hypertrophy, fibrosis, arrhythmias, and infarction. Recent studies on genetically modified cellular and animal models document a crucial role of Wnt/β-catenin signaling in the molecular pathogenesis of arrhythmogenic cardiomyopathy (AC), an inherited disease of intercalated discs, typically characterized by ventricular arrhythmias and progressive substitution of the myocardium with fibrofatty tissue...
April 27, 2017: Oncotarget
https://www.readbyqxmd.com/read/28502095/the-impact-of-age-and-frailty-on-ventricular-structure-and-function-in-c57bl-6j-mice
#18
H A Feridooni, A E Kane, O Ayaz, A Boroumandi, N Polidovitch, R G Tsushima, R A Rose, S E Howlett
KEY POINTS: Heart size increases with age (called hypertrophy), and its ability to contract declines. However, these reflect average changes that may not be present, or present to the same extent, in all older individuals. That aging happens at different rates is well accepted clinically. People who are aging rapidly are frail and frailty is measured with a 'frailty index'. We quantified frailty with a validated mouse frailty index tool and evaluated the impacts of age and frailty on cardiac hypertrophy and contractile dysfunction...
May 14, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/28499868/exposure-to-particulate-matter-induces-cardiomyocytes-apoptosis-after-myocardial-infarction-through-nf%C3%AE%C2%BAb-activation
#19
Xueling Li, Jin Geng, Yuhan Chen, Fu Chen, Chen Liu, Qiwen Xu, Jinxuan Zhao, Jiaxin Hu, Jun Xie, Biao Xu
Clinical evidence has indicated an increased myocardial infarction (MI) morbidity and mortality after exposure to air pollution (particulate matter<2.5 μm, PM2.5). However, the mechanisms by which PM2.5 aggravates MI remain unknown. Present study was to explore the adverse effect of PM2.5 on myocardium after MI and the potential mechanisms. Male mice with MI surgery were treated with PM2.5 by intranasal instillation. Neonatal mice ventricular myocytes (NMVMs) subjected to hypoxia were also incubated with PM2...
June 17, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28498888/cardiomyocyte-specific-loss-of-mitochondrial-p32-c1qbp-causes-cardiomyopathy-and-activates-stress-responses
#20
Toshiro Saito, Takeshi Uchiumi, Mikako Yagi, Rie Amamoto, Daiki Setoyama, Yuichi Matsushima, Dongchon Kang
Aims: Mitochondria are important organelles, dedicated to energy production. Mitochondrial p32/C1qbp, which functions as an RNA and protein chaperone, interacts with mitochondrial mRNA and is indispensable for mitochondrial function through its regulation of mitochondrial translation in cultured cell lines. However, the precise role of p32/C1qbp in vivo is poorly understood because of embryonic lethality in the systemic p32-deficient mouse. The goal of this study was to examine the physiological function of mitochondrial p32/C1qbp in the heart...
May 11, 2017: Cardiovascular Research
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