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Journal of Molecular and Cellular Cardiology

Lindsey J Anstine, Chris Bobba, Samir Ghadiali, Joy Lincoln
Risk factors of heart valve disease are well defined and prolonged exposure throughout life leads to degeneration and dysfunction in up to 33% of the population. While aortic valve replacement remains the most common need for cardiovascular surgery particularly in those aged over 65, the underlying mechanisms of progressive deterioration are unknown. In other cardiovascular systems, a decline in endothelial cell integrity and function play a major role in promoting pathological changes, and while similar mechanisms have been speculated in the valves, studies to support this are lacking...
October 15, 2016: Journal of Molecular and Cellular Cardiology
Rugmani Padmanabhan Iyer, Lisandra E de Castro Brás, Nicolle L Patterson, Manishabrata Bhowmick, Elizabeth R Flynn, Majdouline Asher, Presley L Cannon, Kristine Y Deleon-Pennell, Gregg B Fields, Merry L Lindsey
Matrix metalloproteinase-9 (MMP-9) is robustly elevated in the first week post-myocardial infarction (MI). Targeted deletion of the MMP-9 gene attenuates cardiac remodeling post-MI by reducing macrophage infiltration and collagen accumulation through increased apoptosis and reduced inflammation. In this study, we used a translational experimental design to determine whether selective MMP-9 inhibition early post-MI would be an effective therapeutic strategy in mice. We enrolled male C57BL/6J mice (3-6months old, n=116) for this study...
October 13, 2016: Journal of Molecular and Cellular Cardiology
Audrey N Chang, Kristine E Kamm, James T Stull
Maintenance of contractile performance of the heart is achieved in part by the constitutive 40% phosphorylation of myosin regulatory light chain (RLC) in sarcomeres. The importance of this extent of RLC phosphorylation for optimal cardiac performance becomes apparent when various mouse models and resultant phenotypes are compared. The absence or attenuation of RLC phosphorylation results in poor performance leading to heart failure, whereas increased RLC phosphorylation is associated with cardiac protection from stresses...
October 11, 2016: Journal of Molecular and Cellular Cardiology
Ilka Lorenzen-Schmidt, Samantha B Clarke, W Glen Pyle
Cardiac myofilaments act as the central contractile apparatus of heart muscle cells. Covalent modification of constituent proteins through phosphorylation is a rapid and powerful mechanism to control myofilament function, and is increasingly seen as a mechanism of disease. While the relationship between protein kinases and cardiac myofilaments has been widely examined, the impact of protein dephosphorylation by protein phosphatases is poorly understood. This review outlines the mechanisms by which the mostly widely expressed protein phosphatases in cardiac myocytes regulate myofilament function, and the emerging role of myofilament-associated protein phosphatases in heart failure...
October 6, 2016: Journal of Molecular and Cellular Cardiology
Shirin Doroudgar, Pearl Quijada, Mathias Konstandin, Kelli Ilves, Kathleen Broughton, Farid G Khalafalla, Alexandria Casillas, Kristine Nguyen, Natalie Gude, Haruhiro Toko, Luis Ornelas, Donna J Thuerauf, Christopher C Glembotski, Mark A Sussman, Mirko Völkers
BACKGROUND: Myocardial infarction is followed by cardiac dysfunction, cellular death, and ventricular remodeling, including tissue fibrosis. S100A4 protein plays multiple roles in cellular survival, and tissue fibrosis, but the relative role of the S100A4 in the myocardium after myocardial infarction is unknown. This study aims to investigate the role of S100A4 in myocardial remodeling and cardiac function following infarct damage. METHODS AND RESULTS: S100A4 expression is low in the adult myocardium, but significantly increased following myocardial infarction...
October 6, 2016: Journal of Molecular and Cellular Cardiology
Pablo H Cutini, María B Rauschemberger, Marisa J Sandoval, Virginia L Massheimer
In this work we investigate whether, despite the procalcific action of alendronate on bone, the drug would be able to regulate in vitro the main cellular events that take part in atherosclerotic lesion generation. Using endothelial cell cultures we showed that Alendronate (1-50μM) acutely enhances nitric oxide production (10-30min). This stimulatory action of the bisphosphonate involves the participation of MAPK signaling transduction pathway. Under inflammatory stress, the drug reduces monocytes and platelets interactions with endothelial cells induced by lipopolysaccharide...
October 2, 2016: Journal of Molecular and Cellular Cardiology
Martin Laasmaa, Rikke Birkedal, Marko Vendelin
In cardiac excitation-contraction coupling (ECC), calcium enters the cytosol via L-type Ca(2+) channels (LTCC) and reverse Na(+)/Ca(2+)-exchange (NCXrev), or is released from the sarcoplasmic reticulum (SR) by Ca(2+)-induced Ca(2+)-release (CICR). The magnitude of Ca(2+) influx via the different pathways varies with the state of the cell and is difficult to assess quantitatively, because changes in Ca(2+) influx through one pathway affects the others. In rainbow trout ventricular myocytes, the role of the SR has been uncertain for decades...
October 1, 2016: Journal of Molecular and Cellular Cardiology
Yong Seon Choi, Ana Barbosa Marcondes de Mattos, Dan Shao, Tao Li, Miranda Nabben, Maengjo Kim, Wang Wang, Rong Tian, Stephen C Kolwicz
RATIONALE: Diastolic dysfunction is a common feature in many heart failure patients with preserved ejection fraction and has been associated with altered myocardial metabolism in hypertensive and diabetic patients.Therefore, metabolic interventions to improve diastolic function are warranted.In mice with a germline cardiac-specific deletion of acetyl CoA carboxylase 2 (ACC2), systolic dysfunction induced by pressure-overload was prevented by maintaining cardiac fatty acid oxidation (FAO)...
September 28, 2016: Journal of Molecular and Cellular Cardiology
Wataru Mizushima, Hidehisa Takahashi, Masashi Watanabe, Shintaro Kinugawa, Shouji Matsushima, Shingo Takada, Takashi Yokota, Takaaki Furihata, Junichi Matsumoto, Masaya Tsuda, Ikuru Chiba, Shun Nagashima, Shigeru Yanagi, Masaki Matsumoto, Keiichi I Nakayama, Hiroyuki Tsutsui, Shigetsugu Hatakeyama
A failing heart shows severe energy insufficiency, and it is presumed that this energy shortage plays a critical role in the development of cardiac dysfunction. However, little is known about the mechanisms that cause energy metabolic alterations in the failing heart. Here, we show that the novel RING-finger protein 207 (RNF207), which is specifically expressed in the heart, plays a role in cardiac energy metabolism. Depletion of RNF207 in neonatal rat cardiomyocytes (NRCs) leads to a reduced cellular concentration of adenosine triphosphate (ATP) and mitochondrial dysfunction...
September 25, 2016: Journal of Molecular and Cellular Cardiology
Michael V G Latronico, Gianluigi Condorelli
No abstract text is available yet for this article.
September 21, 2016: Journal of Molecular and Cellular Cardiology
David Y Chiang, Albert J R Heck, Dobromir Dobrev, Xander H T Wehrens
Reversible phosphorylation of proteins is a delicate yet dynamic balancing act between kinases and phosphatases, the disturbance of which underlies numerous disease processes. While our understanding of protein kinases has grown tremendously over the past decades, relatively little is known regarding protein phosphatases. This may be because protein kinases are great in number and relatively specific in function, and thereby amenable to be studied in isolation, whereas protein phosphatases are much less abundant and more unspecific in their function...
September 20, 2016: Journal of Molecular and Cellular Cardiology
Raymond D Devine, Clayton M Eichenseer, Loren E Wold
Cardiovascular dysfunction as a result of tumor burden is becoming a recognized complication; however, the mechanisms remain unknown. A murine model of cancer cachexia has shown marked increases of matrix metalloproteinases (MMPs), known mediators of cardiac remodeling, in the left ventricle. The extent to which MMPs are involved in remodeling remains obscured. To this end a common antibiotic, minocycline, with MMP inhibitory properties was used to elucidate MMP involvement in tumor induced cardiovascular dysfunction...
September 20, 2016: Journal of Molecular and Cellular Cardiology
Stefan A Mann, Mohammad Imtiaz, Annika Winbo, Annika Rydberg, Matthew D Perry, Jean-Philippe Couderc, Bronislava Polonsky, Scott McNitt, Wojciech Zareba, Adam P Hill, Jamie I Vandenberg
In-silico models of human cardiac electrophysiology are now being considered for prediction of cardiotoxicity as part of the preclinical assessment phase of all new drugs. We ask the question whether any of the available models are actually fit for this purpose. We tested three models of the human ventricular action potential, the O'hara-Rudy (ORD11), the Grandi-Bers (GB10) and the Ten Tusscher (TT06) models. We extracted clinical QT data for LQTS1 and LQTS2 patients with nonsense mutations that would be predicted to cause 50% loss of function in IKs and IKr respectively...
September 20, 2016: Journal of Molecular and Cellular Cardiology
Yuri M Kokoz, Edward V Evdokimovskii, Alexander V Maltsev, Miroslav N Nenov, Olga V Nakipova, Alexey S Averin, Oleg Yu Pimenov, Ilia Y Teplov, Alexey V Berezhnov, Santiago Reyes, Alexey E Alekseev
Sustained cardiac adrenergic stimulation has been implicated in the development of heart failure and ventricular dysrhythmia. Conventionally, α2 adrenoceptors (α2-AR) have been assigned to a sympathetic short-loop feedback aimed at attenuating catecholamine release. We have recently revealed the expression of α2-AR in the sarcolemma of cardiomyocytes and identified the ability of α2-AR signaling to suppress spontaneous Ca(2+) transients through nitric oxide (NO) dependent pathways. Herein, patch-clamp measurements and serine/threonine phosphatase assay revealed that, in isolated rat cardiomyocytes, activation of α2-AR suppressed L-type Ca(2+) current (ICaL) via stimulation of NO synthesis and protein kinase G- (PKG) dependent activation of phosphatase reactions, counteracting isoproterenol-induced β-adrenergic activation...
September 19, 2016: Journal of Molecular and Cellular Cardiology
Adonis Z Wu, Dongzhu Xu, Na Yang, Shien-Fong Lin, Peng-Sheng Chen, Steven E Cala, Zhenhui Chen
AIMS: Phospholamban (PLB) regulates the cardiac Ca(2+)-ATPase (SERCA2a) in sarcoplasmic reticulum (SR). However, the localization of PLB at subcellular sites outside the SR and possible contributions to Ca(2+) cycling remain unknown. We examined the intracellular distribution of PLB and tested whether a pool of PLB exists in the nuclear envelope (NE) that might regulate perinuclear/nuclear Ca(2+) (nCa(2+)) handling in cardiomyocytes (CMs). METHODS AND RESULTS: Using confocal immunofluorescence microscopy and immunoblot analyses of CMs and CM nuclei, we discovered that PLB was highly concentrated in NE...
September 15, 2016: Journal of Molecular and Cellular Cardiology
Silvio Weber, Stefanie Meyer-Roxlau, Ali El-Armouche
Phosphoproteomic studies have shown that about one third of all cardiac proteins are reversibly phosphorylated, affecting virtually every cellular signaling pathway. The reversibility of this process is orchestrated by the opposing enzymatic activity of kinases and phosphatases. Conversely, imbalances in subcellular protein phosphorylation patterns are a hallmark of many cardiovascular diseases including heart failure and cardiac arrhythmias. While numerous studies have revealed excessive beta-adrenergic signaling followed by deregulated kinase expression or activity as a major driver of the latter cardiac pathologies, far less is known about the beta-adrenergic regulation of their phosphatase counterparts...
September 14, 2016: Journal of Molecular and Cellular Cardiology
Ningning Hou, Yihui Liu, Fang Han, Di Wang, Xiaoshuang Hou, Shuting Hou, Xiaodong Sun
AIMS: To determine whether irisin could improve perivascular adipose tissue (PVAT) dysfunction via regulation of the heme oxygenase-1 (HO-1)/adiponectin axis in obesity. MATERIALS AND METHODS: C57BL/6 mice were given chow or a high-fat diet (HFD) with or without treatment with irisin. The concentration-dependent responses of the thoracic aorta with or without PVAT (PVAT+ or PVAT-) to phenylephrine were studied in an organ bath. Protein levels of HO-1 and adiponectin were determined by western blot...
September 13, 2016: Journal of Molecular and Cellular Cardiology
Andre Monteiro da Rocha, Guadalupe Guerrero-Serna, Adam Helms, Carly Luzod, Sergey Mironov, Mark Russell, José Jalife, Sharlene M Day, Gary D Smith, Todd J Herron
AIMS: Mutations of cardiac sarcomere genes have been identified to cause HCM, but the molecular mechanisms that lead to cardiomyocyte hypertrophy and risk for sudden death are uncertain. The aim of this study was to examine HCM disease mechanisms at play during cardiac differentiation of human HCM specific pluripotent stem cells. METHODS AND RESULTS: We generated a human embryonic stem cell (hESC) line carrying a naturally occurring mutation of MYPBC3 (c.2905 +1 G >A) to study HCM pathogenesis during cardiac differentiation...
September 9, 2016: Journal of Molecular and Cellular Cardiology
Christoph Lipps, Jenine H Nguyen, Lukas Pyttel, Thomas L Lynch, Christoph Liebetrau, Ganna Aleshcheva, Sandra Voss, Oliver Dörr, Holger M Nef, Helge Möllmann, Christian W Hamm, Sakthivel Sadayappan, Christian Troidl
Myocardial infarction (MI) leads to loss and degradation of contractile cardiac tissue followed by sterile inflammation of the myocardium through activation and recruitment of innate and adaptive cells of the immune system. Recently, it was shown that cardiac myosin binding protein-C (cMyBP-C), a protein of the cardiac sarcomere, is degraded following MI, releasing a predominant N-terminal 40-kDa fragment (C0C1f) into myocardial tissue and the systemic circulation. We hypothesized that early release of C0C1f contributes to the initiation of inflammation and plays a key role in recruitment and activation of immune cells...
September 8, 2016: Journal of Molecular and Cellular Cardiology
Pierre-Alain Thiebaut, Marie Besnier, Elodie Gomez, Vincent Richard
Protein Tyrosine Phosphatase 1B (PTP1B) is mostly involved in negative regulation of signaling mediated by Tyrosine Kinase Receptors, especially the insulin and leptin receptors. This enzyme thus plays a major role in the development of diseases associated with insulin resistance, such as obesity and diabetes. PTP1B inhibition is currently considered as an attractive treatment of insulin resistance and associated metabolic disorders. In parallel, emerging evidence also suggests that PTP1B is widely expressed in cardiovascular tissues, notably in the heart and the endothelium, and that it could also be a potential treatment of several cardiovascular diseases...
September 2, 2016: Journal of Molecular and Cellular Cardiology
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