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Journal of Molecular and Cellular Cardiology

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
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
Qing Yao, Zhi-Qiang Ke, Shuang Guo, Xiao-Song Yang, Fei-Xue Zhang, Xiu-Fen Liu, Xiao Chen, Hong-Guang Chen, Huan-Ya Ke, Chao Liu
The effects of curcumin on regulating cardiac apoptosis and autophagy were analyzed in diabetic models both in vivo and in vitro. In vivo, experimental diabetes was induced in mice by low-dose STZ injection combined with a high-fat diet. In vitro, cultured H9c2 cardiomyoblasts were exposed to high d-glucose concentrations combined with palmitate. Our results showed that apoptosis was increased and autophagy was suppressed in the hearts of diabetic mice, which was ameliorated by curcumin treatment, ultimately improving cardiac function...
October 4, 2018: Journal of Molecular and Cellular Cardiology
Jiajing Xu, Yoram Rudy
Dynamic conformational changes of ion channel proteins during activation gating determine their function as carriers of current. The relationship between these molecular movements and channel function over the physiological timescale of the action potential (AP) has not been fully established due to limitations of existing techniques. We constructed a library of possible cardiac IKs protein conformations and applied a combination of protein segmentation and energy linearization to study this relationship computationally...
October 4, 2018: Journal of Molecular and Cellular Cardiology
Min Huang, Juan Liu, Yunlu Sheng, Yifan Lv, Jing Yu, Hanmei Qi, Wenjuan Di, Shan Lv, Suming Zhou, Guoxian Ding
BACKGROUND: High-fat diet (HFD) induces cardiac hypertrophy; however, the underlying cellular and molecular mechanisms are yet unclear. In the present study, we investigated the roles of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), an amplifier of local glucocorticoid activity, in the pathogenesis of cardiac dysfunction. METHODS: Male Wistar rats were fed normal chow diet (NC) or HFD and examined the cardiac remolding and functional alteration by echocardiography and histology...
October 3, 2018: Journal of Molecular and Cellular Cardiology
Dipendra Khadka, Hyung-Jin Kim, Gi-Su Oh, AiHua Shen, SeungHoon Lee, Su-Bin Lee, Subham Sharma, Seon Young Kim, Arpana Pandit, Seong-Kyu Choe, Tae Hwan Kwak, Sei-Hoon Yang, Hyuk Sim, Gwang Hyeon Eom, Raekil Park, Hong-Seob So
BACKGROUND: Adriamycin (ADR) is a powerful chemotherapeutic agent extensively used to treat various human neoplasms. However, its clinical utility is hampered due to severe adverse side effects i.e. cardiotoxicity and heart failure. ADR-induced cardiomyopathy (AIC) has been reported to be caused by myocardial damage and dysfunction through oxidative stress, DNA damage, and inflammatory responses. Nonetheless, the remedies for AIC are even not established. Therefore, we illustrate the role of NAD+ /NADH modulation by NAD(P)H quinone oxidoreductase 1 (NQO1) enzymatic action on AIC...
October 3, 2018: Journal of Molecular and Cellular Cardiology
Hailey J Jansen, Martin Mackasey, Motahareh Moghtadaei, Darrell D Belke, Emmanuel E Egom, Jari M Tuomi, Sara A Rafferty, Adam W Kirkby, Robert A Rose
Atrial fibrillation (AF) is prevalent in hypertension and elevated angiotensin II (Ang II); however, the mechanisms by which Ang II leads to AF are poorly understood. Here, we investigated the basis for this in mice treated with Ang II or saline for 3 weeks. Ang II treatment increased susceptibility to AF compared to saline controls in association with increases in P wave duration and atrial effective refractory period, as well as reductions in right and left atrial conduction velocity. Patch-clamp studies demonstrate that action potential (AP) duration was prolonged in right atrial myocytes from Ang II treated mice in association with a reduction in repolarizing K+ currents...
September 28, 2018: Journal of Molecular and Cellular Cardiology
Ludmila S Peres Diaz, Mariano Luis Schuman, Maia Aisicovich, Jorge Eduardo Toblli, Carlos José Pirola, María Silvina Landa, Silvia Inés García
Cardiac tyhrotropin-releasing hormone (TRH) is overexpressed in the hypertrophied left ventricle (LV) of spontaneously hypertensive rats (SHR) and its inhibition prevents both hypertrophy and fibrosis. In a normal heart, the TRH increase induces fibrosis and hypertrophy opening the question of whether TRH could be a common mediator of left ventricular hypertrophy (LVH). We used angiotensin II (AngII) as an inductor of LVH to evaluate if the blockade of LV-TRH prevents hypertrophy and fibrosis in mice. We challenged C57BL/6 adult male mice with an infusion of AngII (osmotic pumps; 2 mg/kg...
September 27, 2018: Journal of Molecular and Cellular Cardiology
Yaozhong Liu, Qiman Shi, Yingxu Ma, Qiming Liu
Atrial fibrillation (AF) is the most common sustained arrhythmia, but its mechanisms are poorly understood. Recently, accumulating evidence indicates a link between immune response and AF, but the precise mechanism remains unclear. It should be noticed that the relationship between immune response and AF is complex. Whether immune response is a cause or a result of AF is unclear. As the functional unit of the immune system, immune cells may play a vital role in the immunological pathogenesis of AF. In this review, we briefly highlight the evidence on relationships between immune cells and AF, and discuss their potential roles in AF pathogenesis...
September 26, 2018: Journal of Molecular and Cellular Cardiology
Mu Chen, Dongzhu Xu, Adonis Z Wu, Evangelia Kranias, Shien-Fong Lin, Peng-Sheng Chen, Zhenhui Chen
AIMS: Phospholamban (PLB) is the key regulator of the cardiac Ca2+ pump (SERCA2a)-mediated sarcoplasmic reticulum Ca2+ stores. We recently reported that PLB is highly concentrated in the nuclear envelope (NE) from where it can modulate perinuclear Ca2+ handling of the cardiomyocytes (CMs). Since inositol 1,4,5-trisphosphate (IP3 ) receptor (IP3 R) mediates nuclear Ca2+ release, we examined whether the nuclear pool of PLB regulates IP3 -induced nuclear Ca2+ handling. METHODS AND RESULTS: Fluo-4 based confocal Ca2+ imaging was performed to measure Ca2+ dynamics across both nucleus and cytosol in saponin-permeabilized CMs isolated from wild-type (WT) or PLB-knockout (PLB-KO) mice...
September 24, 2018: Journal of Molecular and Cellular Cardiology
Bence Hegyi, Tamás Bányász, Leighton T Izu, Luiz Belardinelli, Donald M Bers, Ye Chen-Izu
Late Na+ current (INaL ) significantly contributes to shaping cardiac action potentials (APs) and increased INaL is associated with cardiac arrhythmias. β-adrenergic receptor (βAR) stimulation and its downstream signaling via protein kinase A (PKA) and Ca2+ /calmodulin-dependent protein kinase II (CaMKII) pathways are known to regulate INaL . However, it remains unclear how each of these pathways regulates INaL during the AP under physiological conditions. Here we performed AP-clamp experiments in rabbit ventricular myocytes to delineate the impact of each signaling pathway on INaL at different AP phases to understand the arrhythmogenic potential...
September 18, 2018: Journal of Molecular and Cellular Cardiology
Hiroyuki Kawagishi, Jianhua Xiong, Ilsa I Rovira, Haihui Pan, Ye Yan, Bernd K Fleischmann, Mitsuhiko Yamada, Toren Finkel
Certain organisms, including zebrafish, are capable of complete cardiac regeneration in response to injury. This response has also been observed in newborn mice, although in this case, the regenerative capacity is lost at approximately one week of age. The mechanisms regulating this short temporal window of cardiac regeneration in mice are not well understood. Here, we show that sonic hedgehog (Shh) signaling modulates the neonatal mouse regenerative response. In particular, we demonstrate that following apical resection of the heart on postnatal day 1, mice activate Shh ligand expression and downstream signaling...
September 17, 2018: Journal of Molecular and Cellular Cardiology
Shuai Yang, Zi-Ming Ye, Shengcai Chen, Xue-Ying Luo, Shao-Li Chen, Ling Mao, Yanan Li, Huijuan Jin, Cheng Yu, Fei-Xiang Xiang, Ming-Xing Xie, Jiang Chang, Yuan-Peng Xia, Bo Hu
Disruption of carotid vulnerable atherosclerotic plaque is responsible for acute ischemic stroke (AIS) and the early detection and intervention approach are greatly limited. Undertaking a microarray of microRNAs (miRNAs) in the plasma of AIS patients with carotid vulnerable plaques, miR-23a-5p was markedly elevated and was positively correlated with the plaque progression and vulnerability. Correspondingly, we found that miR-23a-5p expression was significantly increased in both plasma and macrophages from atherosclerosis mice...
September 15, 2018: Journal of Molecular and Cellular Cardiology
Qinshuo Zhao, Jingqiu Huang, Dong Wang, Liang Chen, Dating Sun, Chunxia Zhao
BACKGROUND: Myocardial infarction (MI) contributes to the development of cardiac remodeling and heart failure. Insufficient post-MI myocardial angiogenesis has been identified as a non-negligible event which precipitates heart failure progression. Previous studies reported that cytochrome P450 epoxygenase and its metabolites exerted beneficial effects on cardiovascular diseases. However, the role of cytochrome P450 2J2 (CYP2J2) in post-MI heart failure is incompletely understood. METHODS AND RESULTS: First, western blot and real-time PCR analyses showed that CYP2J2 expression increased clearly in patients with acute MI and old MI, compared to control...
September 13, 2018: Journal of Molecular and Cellular Cardiology
Cheng-Chih Chung, Yung-Kuo Lin, Yao-Chang Chen, Yu-Hsun Kao, Yung-Hsin Yeh, Yi-Jen Chen
BACKGROUND: Rivaroxaban, a widely used factor Xa inhibitor in reducing stroke in atrial fibrillation (AF) patients has multiple biological effects with activation of protease-activated receptor (PAR) signaling. Atrial fibrosis plays a critical role in the pathophysiology of AF. In this study, we evaluated whether rivaroxaban regulates atrial fibroblast activity and its underlying mechanisms. METHODS AND RESULTS: Migration, proliferation analyses, nitric oxide (NO) production assay, calcium fluorescence imaging, and western blots were conducted in human atrial fibroblasts with or without rivaroxaban (100 nmol/L or 300 nmol/L) and co-administration of L-NAME (L-NG-nitro arginine methyl ester, 100 μmol/L), EGTA (Ethylene glycol tetra-acetic acid, 1 mmol/L), thrombin (0...
September 10, 2018: Journal of Molecular and Cellular Cardiology
Yidong Wang, Pengfei Lu, Bingruo Wu, Dario F Riascos-Bernal, Nicholas E S Sibinga, Tomas Valenta, Konrad Basler, Bin Zhou
Abnormal endocardial cushion formation is a major cause of congenital heart valve disease, which is a common birth defect with significant morbidity and mortality. Although β-catenin and BMP2 are two well-known regulators of endocardial cushion formation, their interaction in this process is largely unknown. Here, we report that deletion of β-catenin in myocardium results in formation of hypoplastic endocardial cushions accompanying a decrease of mesenchymal cell proliferation. Loss of β-catenin reduced Bmp2 expression in myocardium and SMAD signaling in cushion mesenchyme...
September 8, 2018: Journal of Molecular and Cellular Cardiology
Johann P Kuhtz-Buschbeck, Angela Drake-Holland, Mark I M Noble, Brigitte Lohff, Jochen Schaefer
No abstract text is available yet for this article.
September 7, 2018: Journal of Molecular and Cellular Cardiology
R A Cáceres, T Chavez, D Maestro, A R Palanca, P Bolado, F Madrazo, A Aires, A L Cortajarena, A V Villar
Myocardial fibroblast activation coupled with extracellular matrix production is a pathological signature of myocardial fibrosis and is governed mainly by transforming growth factor TGFβ-Smad2/3 signaling. Targeting the ubiquitous TGFβ leads to cellular homeostasis deregulation with adverse consequences. We previously showed the anti-fibrotic effects upon downregulation of 90-kDa heat shock protein (Hsp90), a chaperone that associates to the TGFβ signaling cascade. In the present study, we use a fluorescent-labeled Hsp90 protein inhibitor (CTPR390-488) with specific Hsp90 binding properties to reduce myocardial pro-fibrotic events in vitro and in vivo...
September 5, 2018: Journal of Molecular and Cellular Cardiology
Gang Li, Aditi Khandekar, Tiankai Yin, Stephanie C Hicks, Qiusha Guo, Kentaro Takahashi, Catherine E Lipovsky, Brittany D Brumback, Praveen K Rao, Carla J Weinheimer, Stacey L Rentschler
Several inherited arrhythmias, including Brugada syndrome and arrhythmogenic cardiomyopathy, primarily affect the right ventricle and can lead to sudden cardiac death. Among many differences, right and left ventricular cardiomyocytes derive from distinct progenitors, prompting us to investigate how embryonic programming may contribute to chamber-specific conduction and arrhythmia susceptibility. Here, we show that developmental perturbation of Wnt signaling leads to chamber-specific transcriptional regulation of genes important in cardiac conduction that persists into adulthood...
September 5, 2018: Journal of Molecular and Cellular Cardiology
Zheng Cheng, Mingming Zhang, Jianqiang Hu, Jie Lin, Xinyu Feng, Shanjie Wang, Tingting Wang, Erhe Gao, Haichang Wang, Dongdong Sun
AIMS: Angiotension II (Ang II) plays a central role in the pathogenesis of renin-angiotensin-aldosterone system (RAAS)-induced heart failure. Mst1 exerts its function in cardiomyocytes subjected to pathological stimuli via inhibiting autophagy and aggravating apoptosis, but its role in RAAS-mediated cardiac injury is still unknown. Here, we aimed to determine whether cardiomyocyte-specific Mst1 knockout can alleviate Ang II-induced cardiac injury by improving cardiomyocyte autophagy and whether these functions depend on Ang II receptors...
September 4, 2018: Journal of Molecular and Cellular Cardiology
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