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(Ca2+/calmodulin-dependent protein kinase II OR CaMKII) AND (heart OR cardiac)

Krishna P Subedi, Min-Jeong Son, Bojjibabu Chidipi, Seong-Woo Kim, Jun Wang, Kyeong-Hee Kim, Sun-Hee Woo, Joon-Chul Kim
BACKGROUND/AIMS: Endothelin-1 (ET-1) and the α<Sub>1</Sub>-adrenoceptor agonist phenylephrine (PE) activate cAMP response element binding protein (CREB), a transcription factor implicated in cardiac hypertrophy. The signaling pathway involved in CREB activation by these hypertrophic stimuli is poorly understood. We examined signaling pathways for ET-1- or PE-induced cardiac CREB activation. METHODS: Western blotting was performed with pharmacological and genetic interventions in rat ventricular myocytes...
2017: Cellular Physiology and Biochemistry
Yawei Ji, Xin Guo, Zhe Zhang, Zhuyun Huang, Jianghua Zhu, Qing-Hui Chen, Le Gui
Evidence suggests that store-operated Ca2+ entry (SOCE) is involved in the hypertrophy of cardiomyocytes. The signaling mechanisms of SOCE contributing to cardiac hypertrophy following phenylephrine (PE) stimulation are not fully understood. Ca(2+)/calmodulin-dependent protein kinase II δ (CaMKIIδ) plays an important role in regulating intracellular Ca(2+) hemostasis and function in the cardimyocytes. This study is aimed to determine the role of CaMKIIδ in regulating the PE-induced myocardial hypertrophy and the associated molecular signaling mechanisms...
March 2017: Cardiovascular Pathology: the Official Journal of the Society for Cardiovascular Pathology
Martin W Berchtold, Triantafyllos Zacharias, Katarzyna Kulej, Kevin Wang, Raffaela Torggler, Thomas Jespersen, Jau-Nian Chen, Martin R Larsen, Jonas M la Cour
Calmodulin (CaM) is a Ca(2+) binding protein modulating multiple targets, several of which are associated with cardiac pathophysiology. Recently, CaM mutations were linked to heart arrhythmia. CaM is crucial for cell growth and viability, yet the effect of the arrhythmogenic CaM mutations on cell viability, as well as heart rhythm, remains unknown, and only a few targets with relevance for heart physiology have been analyzed for their response to mutant CaM. We show that the arrhythmia-associated CaM mutants support growth and viability of DT40 cells in the absence of WT CaM except for the long QT syndrome mutant CaM D129G...
December 23, 2016: Journal of Biological Chemistry
Morten A Høydal, Tomas O Stølen, Sarah Kettlewell, Lars S Maier, Joan Heller Brown, Tomas Sowa, Daniele Catalucci, Gianluigi Condorelli, Ole J Kemi, Godfrey L Smith, Ulrik Wisløff
Several conditions of heart disease, including heart failure and diabetic cardiomyopathy, are associated with upregulation of cytosolic Ca(2+)/calmodulin-dependent protein kinase II (CaMKIIδC) activity. In the heart, CaMKIIδC isoform targets several proteins involved in intracellular Ca(2+) homeostasis. We hypothesized that high-intensity endurance training activates mechanisms that enable a rescue of dysfunctional cardiomyocyte Ca(2+) handling and thereby ameliorate cardiac dysfunction despite continuous and chronic elevated levels of CaMKIIδC CaMKIIδC transgenic (TG) and wild-type (WT) mice performed aerobic interval exercise training over 6 wk...
July 1, 2016: Journal of Applied Physiology
Ravinea Manotheepan, Tore K Danielsen, Mani Sadredini, Mark E Anderson, Cathrine R Carlson, Stephan E Lehnart, Ivar Sjaastad, Mathis K Stokke
AIMS: Catecholaminergic polymorphic ventricular tachycardia type 1 (CPVT1) is caused by mutations in the cardiac ryanodine receptor (RyR2) that lead to disrupted Ca(2+) handling in cardiomyocytes and ventricular tachycardia. The aim of this study was to test whether exercise training could reduce the propensity for arrhythmias in mice with the CPVT1-causative missense mutation Ryr2-R2474S by restoring normal Ca(2+) handling. METHODS AND RESULTS: Ryr2-R2474S mice (RyR-RS) performed a 2 week interval treadmill exercise training protocol...
August 1, 2016: Cardiovascular Research
Mani Sadredini, Tore Kristian Danielsen, Jan Magnus Aronsen, Ravinea Manotheepan, Karina Hougen, Ivar Sjaastad, Mathis Korseberg Stokke
Abnormal cellular Ca2+ handling contributes to both contractile dysfunction and arrhythmias in heart failure. Reduced Ca2+ transient amplitude due to decreased sarcoplasmic reticulum Ca2+ content is a common finding in heart failure models. However, heart failure models also show increased propensity for diastolic Ca2+ release events which occur when sarcoplasmic reticulum Ca2+ content exceeds a certain threshold level. Such Ca2+ release events can initiate arrhythmias. In this study we aimed to investigate if both of these aspects of altered Ca2+ homeostasis could be found in left ventricular cardiomyocytes from rats with different states of cardiac function six weeks after myocardial infarction when compared to sham-operated controls...
2016: PloS One
Yuejin Wu, Héctor H Valdivia, Xander H T Wehrens, Mark E Anderson
BACKGROUND: Fight or flight heart rate (HR) increases depend on protein kinase A (PKA)- and calmodulin kinase II (CaMKII)-mediated enhancement of Ca(2+) uptake and release from sarcoplasmic reticulum (SR) in sinoatrial nodal cells (SANC). However, the impact of specific PKA and CaMKII phosphorylation sites on HR is unknown. METHODS AND RESULTS: We systematically evaluated validated PKA and CaMKII target sites on phospholamban and the ryanodine receptor using genetically modified mice...
February 2016: Circulation. Arrhythmia and Electrophysiology
Leandro Sommese, Carlos A Valverde, Paula Blanco, María Cecilia Castro, Omar Velez Rueda, Marcia Kaetzel, John Dedman, Mark E Anderson, Alicia Mattiazzi, Julieta Palomeque
BACKGROUND: Heart failure and arrhythmias occur more frequently in patients with type 2 diabetes (T2DM) than in the general population. T2DM is preceded by a prediabetic condition marked by elevated reactive oxygen species (ROS) and subclinical cardiovascular defects. Although multifunctional Ca2+ calmodulin-dependent protein kinase II (CaMKII) is ROS-activated and CaMKII hyperactivity promotes cardiac diseases, a link between prediabetes and CaMKII in the heart is unprecedented. OBJECTIVES: To prove the hypothesis that increased ROS and CaMKII activity contribute to heart failure and arrhythmogenic mechanisms in early stage diabetes...
January 1, 2016: International Journal of Cardiology
Kazuya Mizukami, Hisashi Yokoshiki, Hirofumi Mitsuyama, Masaya Watanabe, Taro Tenma, Shingo Takada, Hiroyuki Tsutsui
Left ventricular hypertrophy is associated with an increased risk of ventricular arrhythmias. However, the underlying molecular basis is poorly understood. It has been reported that small-conductance Ca(2+)-activated K(+) (SK) channels are involved in the pathogenesis of ventricular arrhythmias in heart failure. The present study aimed to test the hypothesis that SK channel activity is increased via the Ca(2+)/calmodulin-dependent protein kinase II (CaMKII)-dependent pathway in hypertensive cardiac hypertrophy...
September 15, 2015: American Journal of Physiology. Heart and Circulatory Physiology
Beatriz Merino, Ivan Quesada, Jesús Hernández-Cascales
This study evaluated the chronotropic and inotropic responses to glucagon in spontaneously beating isolated right atria of rat heart. For comparison, we also investigated the effects resulting from stimulating β-adrenoceptors with isoproterenol in this tissue. Isoproterenol increased both atrial frequency and contractility but glucagon only enhanced atrial rate. The transcript levels of glucagon receptors were about three times higher in sinoatrial node than in the atrial myocardium. Chronotropic responses to glucagon and isoproterenol were blunted by the funny current (If) inhibitor ZD 7288...
2015: PloS One
Lei Liu, Chao Wang, Dianjun Sun, Shuangquan Jiang, Hong Li, Weihua Zhang, Yajun Zhao, Yuhui Xi, Sa Shi, Fanghao Lu, Ye Tian, Changqing Xu, Lina Wang
BACKGROUND/AIMS: Intracellular calcium concentration ([Ca2+]i) homeostasis, an initial factor of cardiac hypertrophy, is regulated by the calcium-sensing receptor (CaSR) and is associated with the formation of autolysosomes. The aim of this study was to investigate the role of Calhex231, a CaSR inhibitor, on the hypertrophic response via autophagy modulation. METHODS: Cardiac hypertrophy was induced by transverse aortic constriction (TAC) in 40 male Wistar rats, while 10 rats underwent a sham operation and served as controls...
2015: Cellular Physiology and Biochemistry
Ersilia Cipolletta, Maria Rosaria Rusciano, Angela Serena Maione, Gaetano Santulli, Daniela Sorriento, Carmine Del Giudice, Michele Ciccarelli, Antonietta Franco, Catherine Crola, Pietro Campiglia, Marina Sala, Isabel Gomez-Monterrey, Nicola De Luca, Bruno Trimarco, Guido Iaccarino, Maddalena Illario
AIMS: Activation of Ca2+/Calmodulin protein kinase II (CaMKII) is an important step in signaling of cardiac hypertrophy. The molecular mechanisms by which CaMKII integrates with other pathways in the heart are incompletely understood. We hypothesize that CaMKII association with extracellular regulated kinase (ERK), promotes cardiac hypertrophy through ERK nuclear localization. METHODS AND RESULTS: In H9C2 cardiomyoblasts, the selective CaMKII peptide inhibitor AntCaNtide, its penetratin conjugated minimal inhibitory sequence analog tat-CN17β, and the MEK/ERK inhibitor UO126 all reduce phenylephrine (PE)-mediated ERK and CaMKII activation and their interaction...
2015: PloS One
Thomas H Fischer, Jonas Herting, Fleur E Mason, Nico Hartmann, Saera Watanabe, Viacheslav O Nikolaev, Julia U Sprenger, Peidong Fan, Lina Yao, Aron-Frederik Popov, Bernhard C Danner, Friedrich Schöndube, Luiz Belardinelli, Gerd Hasenfuss, Lars S Maier, Samuel Sossalla
AIMS: Enhanced cardiac late Na current (late INa) and increased sarcoplasmic reticulum (SR)-Ca(2+)-leak are both highly arrhythmogenic. This study seeks to identify signalling pathways interconnecting late INa and SR-Ca(2+)-leak in atrial cardiomyocytes (CMs). METHODS AND RESULTS: In murine atrial CMs, SR-Ca(2+)-leak was increased by the late INa enhancer Anemonia sulcata toxin II (ATX-II). An inhibition of Ca(2+)/calmodulin-dependent protein kinase II (Autocamide-2-related inhibitory peptide), protein kinase A (H89), or late INa (Ranolazine or Tetrodotoxin) all prevented ATX-II-dependent SR-Ca(2+)-leak...
July 1, 2015: Cardiovascular Research
Patrick Lugenbiel, Fabian Wenz, Katharina Govorov, Patrick A Schweizer, Hugo A Katus, Dierk Thomas
Atrial fibrillation (AF) and heart failure (HF) are two of the most common cardiovascular diseases. They often coexist and account for significant morbidity and mortality. Alterations in cellular Ca2+ homeostasis play a critical role in AF initiation and maintenance. This study was designed to specifically elucidate AF-associated remodeling of atrial Ca2+ cycling in the presence of mild HF. AF was induced in domestic pigs by atrial burst pacing. The animals underwent electrophysiologic and echocardiographic examinations...
2015: PloS One
Eva Poláková, Ardo Illaste, Ernst Niggli, Eric A Sobie
KEY POINTS: Refractoriness of calcium release in heart cells is altered in several disease states, but the physiological mechanisms that regulate this process are incompletely understood. We examined refractoriness of calcium release in mouse ventricular myocytes and investigated how activation of different intracellular signalling pathways influenced this process. We found that refractoriness of calcium release is abbreviated by stimulation of the 'fight-or-flight' response, and that simultaneous activation of multiple intracellular signalling pathways contributes to this response...
March 15, 2015: Journal of Physiology
Malik Bisserier, Magali Berthouze-Duquesnes, Magali Breckler, Florence Tortosa, Loubina Fazal, Annélie de Régibus, Anne-Coline Laurent, Audrey Varin, Alexandre Lucas, Maxime Branchereau, Pauline Marck, Jean-Nicolas Schickel, Claudine Deloménie, Olivier Cazorla, Pauline Soulas-Sprauel, Bertrand Crozatier, Eric Morel, Christophe Heymes, Frank Lezoualc'h
BACKGROUND: Cardiac hypertrophy is an early hallmark during the clinical course of heart failure and is regulated by various signaling pathways. However, the molecular mechanisms that negatively regulate these signal transduction pathways remain poorly understood. METHODS AND RESULTS: Here, we characterized Carabin, a protein expressed in cardiomyocytes that was downregulated in cardiac hypertrophy and human heart failure. Four weeks after transverse aortic constriction, Carabin-deficient (Carabin(-/-)) mice developed exaggerated cardiac hypertrophy and displayed a strong decrease in fractional shortening (14...
January 27, 2015: Circulation
Eugene E Kim, Akshay Shekhar, Jia Lu, Xianming Lin, Fang-Yu Liu, Jie Zhang, Mario Delmar, Glenn I Fishman
Cardiac Purkinje cells are important triggers of ventricular arrhythmias associated with heritable and acquired syndromes; however, the mechanisms responsible for this proarrhythmic behavior are incompletely understood. Here, through transcriptional profiling of genetically labeled cardiomyocytes, we identified expression of Purkinje cell protein-4 (Pcp4), a putative regulator of calmodulin and Ca2+/calmodulin-dependent kinase II (CaMKII) signaling, exclusively within the His-Purkinje network. Using Pcp4-null mice and acquired cardiomyopathy models, we determined that reduced expression of PCP4 is associated with CaMKII activation, abnormal electrophysiology, dysregulated intracellular calcium handling, and proarrhythmic behavior in isolated Purkinje cells...
November 2014: Journal of Clinical Investigation
Serge Viatchenko-Karpinski, Dmytro Kornyeyev, Nesrine El-Bizri, Grant Budas, Peidong Fan, Zhan Jiang, Jin Yang, Mark E Anderson, John C Shryock, Ching-Pin Chang, Luiz Belardinelli, Lina Yao
An increase of late Na(+) current (INaL) in cardiac myocytes can raise the cytosolic Na(+) concentration and is associated with activation of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) and alterations of mitochondrial metabolism and Ca(2+) handling by sarcoplasmic reticulum (SR). We tested the hypothesis that augmentation of INaL can increase mitochondrial reactive oxygen species (ROS) production and oxidation of CaMKII, resulting in spontaneous SR Ca(2+) release and increased diastolic Ca(2+) in myocytes...
November 2014: Journal of Molecular and Cellular Cardiology
Ru-Jia Liao, Li-Juan Tong, Chao Huang, Wen-Wen Cao, Yu-Zhe Wang, Jia Wang, Xiang-Fan Chen, Wei-Zhong Zhu, Wei Zhang
Our previous studies showed that protein phosphatase 1γ (PP1γ) exacerbates cardiomyocyte apoptosis through promotion of Ca(2+)/calmodulin-dependent protein kinase δ (CaMKIIδ) splicing. Here we determine the role of PP1γ in abdominal aorta constriction-induced hypertrophy and remodelling in rat hearts. Systolic blood pressure and echocardiographic measurements were used to evaluate the model of cardiac hypertrophy. Sirius red staining and invasive haemodynamic/cardiac index measurements were used to evaluate the effects of PP1γ or inhibitor 1 of PP1 transfection...
December 2014: Clinical and Experimental Pharmacology & Physiology
Luis Alberto Gonano, Martín Vila Petroff
Cardiotonic glycosides or digitalis are positive inotropes used in clinical practice for the treatment of heart failure, which also exist as endogenous ligands of the Na(+)/K(+) ATPase. An increase in the intracellular Ca2+ content mediates their positive inotropic effect, but has also been proposed as a trigger of life-threatening arrhythmias. Although the mechanisms involved in the positive inotropic effect of these compounds have been extensively studied, those underlying their arrhythmogenic action remain ill defined...
December 2014: Heart, Lung & Circulation
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