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Journal of Molecular and Cellular Cardiology

Cong Li, Jing Li, Ke Xue, Jun Zhang, Cong Wang, Qingqing Zhang, Xianlu Chen, Chuanzhou Gao, Xiao Yu, Lei Sun
Myocardial infarction (MI) is one of the most catastrophic diseases threatening human health in the world. Because cardiomyocytes have a minuscule regenerative potential, the natural repair of infarct healing after MI shows fibrotic scar. MicroRNA-143-3p (miR-143-3p) plays a critical regulatory role in various pathophysiological processes in the heart. Sprouty3 (SPRY3) is predicted to be a potential fibrosis-associated target gene of miR-143-3p. The aim was to explore the role and mechanism of miR-143-3p in the infarct healing after MI in vivo and in vitro...
March 13, 2019: Journal of Molecular and Cellular Cardiology
Giovanna Gallo, Vivianne Presta, Massimo Volpe, Speranza Rubattu
Aortic valve stenosis (AS) is the most common heart valve disease in North America and Europe leading to an increased risk of heart failure and death. A multidisciplinary evaluation of symptoms, individual risk profile, echocardiographic parameters, biomarkers assessment is required for an appropriate clinical and therapeutic management of AS. The natriuretic peptides (NPs) represent an important biomarker for diagnostic, prognostic and therapeutic purposes in several cardiovascular diseases. The present review article provides an overview of the current knowledge on the role of NPs in the pathogenesis, diagnosis, risk stratification and potential therapeutic implications in AS...
March 13, 2019: Journal of Molecular and Cellular Cardiology
Lidong Cai, Baozhen Qi, Xiaoyu Wu, Shi Peng, Genqing Zhou, Yong Wei, Juan Xu, Songwen Chen, Shaowen Liu
The apoptotic death of cardiomyocytes critically contributes to cardiac remodeling after myocardial infarction (MI). Circular RNAs (circRNAs) are important regulators for a variety of biological functions. Circ-Ttc3 represents one of the top highest expressed circRNAs in the heart; however, its role in MI remains unknown. Herein, we found that circ-Ttc3 was markedly upregulated in the ischemic myocardium and the cardiomyocytes subjected to hypoxic insult. Forced expression of circ-Ttc3 in cardiomyocytes counteracted hypoxia-induced ATP depletion and apoptotic death, in sharp contrast to circ-Ttc3 knockdown...
March 12, 2019: Journal of Molecular and Cellular Cardiology
Paolo Magni
Bicuspid aortic valve (BAV) is recognized as a syndrome including aortic valve diseases and aortic wall alterations, such as aortic dilatation, dissection and rupture, but also coronary atherosclerosis. The current evidence, although partially controversial, suggests that several molecular mechanisms promoting atherosclerosis are activated in BAV patients and are involved in the progression of the related diseases, from aortic stenosis to aortopathies, along with altered hemodynamics. Among these factors, dyslipidemia (i...
March 11, 2019: Journal of Molecular and Cellular Cardiology
David Y Barefield, James W McNamara, Thomas L Lynch, Diederik W D Kuster, Suresh Govindan, Lauren Haar, Yang Wang, Erik N Taylor, John N Lorenz, Michelle L Nieman, Guangshuo Zhu, Pradeep K Luther, Andras Varró, Dobromir Dobrev, Xun Ai, Paul M L Janssen, David A Kass, Walter Keith Jones, Richard J Gilbert, Sakthivel Sadayappan
Cardiac myosin binding protein-C (cMyBP-C) phosphorylation is essential for normal heart function and protects the heart from ischemia-reperfusion (I/R) injury. It is known that protein kinase-A (PKA)-mediated phosphorylation of cMyBP-C prevents I/R-dependent proteolysis, whereas dephosphorylation of cMyBP-C at PKA sites correlates with its degradation. While sites on cMyBP-C associated with phosphorylation and proteolysis co-localize, the mechanisms that link cMyBP-C phosphorylation and proteolysis during cardioprotection are not well understood...
March 9, 2019: Journal of Molecular and Cellular Cardiology
Chenghui Zhou, Yu Chen, Wenying Kang, Hong Lv, Zhongrong Fang, Fuxia Yan, Lihuan Li, Weili Zhang, Jia Shi
OBJECTIVE: To analyze the effects of miR-455-3p-1 and its possible mechanisms in pulmonary arterial hypertension (PAH). METHODS: A microarray assay was used to examine the expressed genes between normal and PAH. The expressed genes in PAH was assessed by qRT-PCR. The targeted interaction between miRNAs and FGF7 was confirmed using a dual luciferase reporter assay. A CCK-8 assay and cell count were used to analyze the pulmonary artery smooth muscle cells (PASMCs) activity and proliferation level, respectively...
March 8, 2019: Journal of Molecular and Cellular Cardiology
Rachel Nordgren
No abstract text is available yet for this article.
March 7, 2019: Journal of Molecular and Cellular Cardiology
Lucía Alonso-Carbajo, Yeranddy A Alpizar, Justyna B Startek, José Ramón López-López, María Teresa Pérez-García, Karel Talavera
The Transient Receptor Potential Melastatin 3 (TRPM3) is a Ca2+ -permeable non-selective cation channel activated by the neurosteroid pregnenolone sulfate (PS). This compound was previously shown to contract mouse aorta by activating TRPM3 in vascular smooth muscle cells (VSMC), and proposed as therapeutic modulator of vascular functions. However, PS effects and the role of TRPM3 in resistance arteries remain unknown. Thus, we aimed at determining the localization and physiological role of TRPM3 in mouse mesenteric arteries...
March 7, 2019: Journal of Molecular and Cellular Cardiology
Brian R Thompson, Kailey J Soller, Anthony Vetter, Jing Yang, Gianluigi Veglia, Michael T Bowser, Joseph M Metzger
Nucleic acid - protein interactions are critical for regulating gene activation in the nucleus. In the cytoplasm, however, potential nucleic acid-protein functional interactions are less clear. The emergence of a large and expanding number of non-coding RNAs and DNA fragments raises the possibility that the cytoplasmic nucleic acids may interact with cytoplasmic cellular components to directly alter key biological processes within the cell. We now show that both natural and synthetic nucleic acids, collectively XNAs, when introduced to the cytoplasm of live cell cardiac myocytes, markedly enhance contractile function via a mechanism that is independent of new translation, activation of the TLR-9 pathway or by altered intracellular Ca2+ cycling...
March 5, 2019: Journal of Molecular and Cellular Cardiology
Rachel Nordgren
No abstract text is available yet for this article.
March 4, 2019: Journal of Molecular and Cellular Cardiology
Mihály Ruppert, Beáta Bódi, Sevil Korkmaz-Icöz, Sivakkanan Loganathan, Weipeng Jiang, Lorenz Lehmann, Attila Oláh, Bálint András Barta, Alex Ali Sayour, Béla Merkely, Matthias Karck, Zoltán Papp, Gábor Szabó, Tamás Radovits
AIM: Here we aimed at investigating the relation between left ventricular (LV) contractility and myofilament function during the development and progression of pressure overload (PO)-induced LV myocardial hypertrophy (LVH). METHODS: Abdominal aortic banding (AB) was performed to induce PO in rats for 6, 12 and 18 weeks. Sham operated animals served as controls. Structural and molecular alterations were investigated by serial echocardiography, histology, quantitative real-time PCR and western blot...
March 4, 2019: Journal of Molecular and Cellular Cardiology
Yuguang Zhao, Wenjing Song, Lizhe Wang, Madhavi J Rane, Fujun Han, Lu Cai
Although there is an increasing understanding of the signaling pathways that promote cardiac hypertrophy, negative regulatory factors of this process have received less attention. Increasing evidence indicates that Krüppel-like factor 15 (KLF15) plays an important role in maintaining cardiac function by controlling the transcriptional pathways that regulating cardiac metabolism. Recent studies have also revealed a vital role for KLF15 as an inhibitor of pathological cardiac hypertrophy and fibrosis via its effects on factors such as myocyte enhancer factor 2 (MEF2), GATA-binding protein 4 (GATA4), transforming growth factor-β (TGF-β), and myocardin...
March 1, 2019: Journal of Molecular and Cellular Cardiology
Iolanda Aquila, Giacomo Frati, Sebastiano Sciarretta, Santo Dellegrottaglie, Daniele Torella, Michele Torella
Bicuspid aortic valve (BAV) disease is the most common congenital cardiac malformation associated with an increased lifetime risk and a high rate of surgically-relevant valve deterioration and aortic dilatation. Genomic data revealed that different genes are associated with BAV. A dominant genetic factor for the recent past was the basis to the recommendation for a more extensive aortic intervention. However very recent evidence that hemodynamic stressors and alterations of wall shear stress play an important role independent from the genetic trait led to more conservative treatment recommendations...
February 28, 2019: Journal of Molecular and Cellular Cardiology
Min Xie, Yida Tang, Joseph A Hill
Reperfusion injury during myocardial infarction accounts for approximately half of final infarct size. Whereas this has been known for decades, efficacious therapy targeting reperfusion injury remains elusive. Many proteins are subject to reversible acetylation, and drugs targeting enzymes that govern these events have emerged in oncology. Among these, small molecules targeting protein deacetylating enzymes, so-called histone deacetylases, are approved for human use in rare cancers. Now, work emerging from multiple laboratories, and in both mice and large animals, has documented that HDAC inhibition using compounds approved for clinical use confers robust cardioprotection when delivered at the time of myocardial reperfusion...
February 27, 2019: Journal of Molecular and Cellular Cardiology
Amalia Forte, Carmela Rita Balistreri, Marisa De Feo, Alessandro Della Corte, Per Hellstrand, Lo Persson, Bengt-Olof Nilsson
Polyamines are small aliphatic cationic molecules synthesized via a highly regulated pathway and involved in general molecular and cellular phenomena. Both mammalian cells and microorganisms synthesize polyamines, and both sources may contribute to the presence of polyamines in the circulation. The dominant location for microorganisms within the body is the gut. Accordingly, the gut microbiota probably synthesizes most of the polyamines in the circulation in addition to those produced by the mammalian host cells...
February 27, 2019: Journal of Molecular and Cellular Cardiology
Dharendra Thapa, Bingxian Xie, Manling Zhang, Michael W Stoner, Janet R Manning, Brydie R Huckestein, Lia R Edmunds, Steven J Mullett, Charles F McTiernan, Stacy G Wendell, Michael J Jurczak, Iain Scott
Exposure to a high fat (HF) diet promotes increased fatty acid uptake, fatty acid oxidation and lipid accumulation in the heart. These maladaptive changes impact cellular energy metabolism and may promote the development of cardiac dysfunction. Attempts to increase cardiac glucose utilization have been proposed as a way to reverse cardiomyopathy in obese and diabetic individuals. Adropin is a nutrient-regulated metabolic hormone shown to promote glucose oxidation over fatty acid oxidation in skeletal muscle homogenates in vitro...
February 26, 2019: Journal of Molecular and Cellular Cardiology
Dawoud Sulaiman, Jingyuan Li, Asokan Devarajan, Christine Marie Cunningham, Min Li, Gregory A Fishbein, Alan M Fogelman, Mansoureh Eghbali, Srinivasa T Reddy
OBJECTIVE: To investigate the novel role of Paraoxonase 2 (PON2) in modulating acute myocardial ischemia-reperfusion injury (IRI). APPROACH: IRI was induced both in vivo and ex vivo in male, C57BL6/J (WT) and PON2-deficient (PON-def) mice. In addition, in vitro hypoxia-reoxygenation injury (HRI) was induced in H9c2 cells expressing empty vector (H9c2-EV) or human PON2 (H9c2-hPON2) ± LY294002 (a potent PI3K inhibitor). Infarct size, PON2 gene expression, mitochondrial calcium retention capacity (CRC), reactive oxygen species (ROS) generation, mitochondrial membrane potential, CHOP and pGSK-3β protein levels, and cell apoptosis were evaluated...
February 23, 2019: Journal of Molecular and Cellular Cardiology
Tian-Tian Wang, Mao-Mao Shi, Xiao-Long Liao, Yu-Quan Li, Hao-Xiang Yuan, Yan Li, Xiang Liu, Da-Sheng Ning, Yue-Ming Peng, Fan Yang, Zhi-Wei Mo, Yu-Mei Jiang, Ying-Qi Xu, Haobo Li, Min Wang, Zhi-Jun Ou, Zhengyuan Xia, Jing-Song Ou
Ischemia postconditioning (PTC) can reduce myocardial ischemia/reperfusion injury. However, the effectiveness of PTC cardioprotection is reduced or lost in diabetes and the mechanisms are largely unclear. Hyperglycemia can induce overexpression of inducible nitric oxide synthesis (iNOS) in the myocardium of diabetic subjects. However, it is unknown whether or not iNOS especially its overexpression plays an important role in the loss of cardioprotection of PTC in diabetes. C57BL6 and iNOS-/- mice were treated with streptozotocin to induce diabetes...
February 21, 2019: Journal of Molecular and Cellular Cardiology
Annika Kluge, Ashraf Yusuf Rangrez, Lucia Sophie Kilian, Jost Pott, Alexander Bernt, Robert Frauen, Astrid Rohrbeck, Norbert Frey, Derk Frank
Cardiac remodeling is induced by mechanical or humoral stress causing pathological changes to the heart. Here, we aimed at identifying the role of differentially regulated genes upon dynamic mechanical stretch. Microarray of dynamic stretch induced neonatal rat ventricular cardiomyocytes (NRVCMs) discovered Rho family GTPase 1 (Rnd1) as one of the significantly upregulated genes, a cardiac role of which is not known yet. Rnd1 was consistently upregulated in NRVCMs after dynamic stretch or phenylephrine (PE) stimulation, and in a mouse model of pressure overload...
February 21, 2019: Journal of Molecular and Cellular Cardiology
Robert Lakin, Nazari Polidovitch, Sibao Yang, Camilo Guzman, Xiaodong Gao, Marianne Wauchop, Peter H Backx
Intense endurance exercise is linked to atrial fibrillation (AF). We established previously that interventions that simultaneously interfere with TNFα signaling, mediated via both the enzymatically liberated soluble and membrane-bound forms of TNFα, prevent atrial remodeling and AF vulnerability in exercised mice. To investigate which signaling modality underlies this protection, we treated exercised mice with XPRO®1595, a selective dominant-negative inhibitor of solTNFα. In male CD1 mice, 6 weeks of intense swim exercise induced reductions in heart rate, increased cardiac vagal tone, left ventricular (LV) dilation and enhanced LV function...
February 20, 2019: Journal of Molecular and Cellular Cardiology
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