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Cardiac Calcium/calmodulin-dependent kinase type II

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https://www.readbyqxmd.com/read/28487342/calcium-calmodulin-dependent-protein-kinase-ii-activity-persists-during-chronic-%C3%AE-adrenoceptor-blockade-in-experimental-and-human-heart-failure
#1
Matthias Dewenter, Stefan Neef, Christiane Vettel, Simon Lämmle, Christina Beushausen, Laura C Zelarayan, Sylvia Katz, Albert von der Lieth, Stefanie Meyer-Roxlau, Silvio Weber, Thomas Wieland, Samuel Sossalla, Johannes Backs, Joan H Brown, Lars S Maier, Ali El-Armouche
BACKGROUND: Considerable evidence suggests that calcium/calmodulin-dependent protein kinase II (CaMKII) overactivity plays a crucial role in the pathophysiology of heart failure (HF), a condition characterized by excessive β-adrenoceptor (β-AR) stimulation. Recent studies indicate a significant cross talk between β-AR signaling and CaMKII activation presenting CaMKII as a possible downstream mediator of detrimental β-AR signaling in HF. In this study, we investigated the effect of chronic β-AR blocker treatment on CaMKII activity in human and experimental HF...
May 2017: Circulation. Heart Failure
https://www.readbyqxmd.com/read/28242257/exendin-4-inhibits-structural-remodeling-and-improves-ca-2-homeostasis-in-rats-with-heart-failure-via-the-glp-1-receptor-through-the-enos-cgmp-pkg-pathway
#2
Jingjing Chen, Dandan Wang, Fangai Wang, Shaobo Shi, Yuting Chen, Bo Yang, Yanhong Tang, Congxin Huang
The glucagon-like peptide-1 receptor (GLP-1R) agonist exendin-4 is a long-acting analog of GLP-1, which stimulates insulin secretion and is clinically used in the treatment of type 2 diabetes. Previous studies have demonstrated that GLP-1 agonists and analogs serve as cardioprotective factors in various conditions. Disturbances in calcium cycling are characteristic of heart failure (HF); therefore, the aim of this study was to investigate the effect of exendin-4 (a GLP-1 mimetic) on the regulation of calcium handling and to identify the underlying mechanisms in an HF rat model after myocardial infarction (MI)...
April 2017: Peptides
https://www.readbyqxmd.com/read/28220073/enhanced-late-na-and-ca-currents-as-effective-antiarrhythmic-drug-targets
#3
REVIEW
Hrayr S Karagueuzian, Arash Pezhouman, Marina Angelini, Riccardo Olcese
While recent advances clarified the molecular and cellular modes of action of antiarrhythmic drugs (AADs), their link to suppression of dynamical arrhythmia mechanisms remains only partially understood. The current classifications of AADs (Classes I, III, and IV) rely on blocking peak Na, K and L-type calcium currents (ICa,L), with Class II with dominant beta receptor blocking activity and Class V including drugs with diverse classes of actions. The discovery that the calcium and redox sensor, cardiac Ca/calmodulin-dependent protein kinase II (CaMKII) enhances both the late Na (INa-L) and the late ICa,L in patients at high risk of VT/VF provided a new and a rational AAD target...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/27864509/loss-of-%C3%AE-adrenergic-stimulated-phosphorylation-of-cav1-2-channels-on-ser1700-leads-to-heart-failure
#4
Linghai Yang, Dao-Fu Dai, Can Yuan, Ruth E Westenbroek, Haijie Yu, Nastassya West, Horacio O de la Iglesia, William A Catterall
L-type Ca(2+) currents conducted by voltage-gated calcium channel 1.2 (CaV1.2) initiate excitation-contraction coupling in the heart, and altered expression of CaV1.2 causes heart failure in mice. Here we show unexpectedly that reducing β-adrenergic regulation of CaV1.2 channels by mutation of a single PKA site, Ser1700, in the proximal C-terminal domain causes reduced contractile function, cardiac hypertrophy, and heart failure without changes in expression, localization, or function of the CaV1.2 protein in the mutant mice (SA mice)...
December 6, 2016: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/27688314/genotype-dependent-and-independent-calcium-signaling-dysregulation-in-human-hypertrophic-cardiomyopathy
#5
Adam S Helms, Francisco J Alvarado, Jaime Yob, Vi T Tang, Francis Pagani, Mark W Russell, Héctor H Valdivia, Sharlene M Day
BACKGROUND: Aberrant calcium signaling may contribute to arrhythmias and adverse remodeling in hypertrophic cardiomyopathy (HCM). Mutations in sarcomere genes may distinctly alter calcium handling pathways. METHODS: We analyzed gene expression, protein levels, and functional assays for calcium regulatory pathways in human HCM surgical samples with (n=25) and without (n=10) sarcomere mutations compared with control hearts (n=8). RESULTS: Gene expression and protein levels for calsequestrin, L-type calcium channel, sodium-calcium exchanger, phospholamban, calcineurin, and calcium/calmodulin-dependent protein kinase type II (CaMKII) were similar in HCM samples compared with controls...
November 29, 2016: Circulation
https://www.readbyqxmd.com/read/27648519/calcium-calmodulin-protein-kinase-ii-dependent-ryanodine-receptor-phosphorylation-mediates-cardiac-contractile-dysfunction-associated-with-sepsis
#6
Marisa Sepúlveda, Luis A Gonano, Manuel Viotti, Malena Morell, Paula Blanco, Micaela López Alarcón, Isalira Peroba Ramos, Adriana Bastos Carvalho, Emiliano Medei, Martín Vila Petroff
OBJECTIVES: Sepsis is associated with cardiac contractile dysfunction attributed to alterations in Ca handling. We examined the subcellular mechanisms involved in sarcoplasmic reticulum Ca loss that mediate altered Ca handling and contractile dysfunction associated with sepsis. DESIGN: Randomized controlled trial. SETTING: Research laboratorySUBJECTS:: Male wild type and transgenic miceINTERVENTIONS:: We induced sepsis in mice using the colon ascendens stent peritonitis model...
April 2017: Critical Care Medicine
https://www.readbyqxmd.com/read/27595734/vasostatin-1-stops-structural-remodeling-and-improves-calcium-handling-via-the-enos-no-pkg-pathway-in-rat-hearts-subjected-to-chronic-%C3%AE-adrenergic-receptor-activation
#7
Dandan Wang, Yingguang Shan, Yan Huang, Yanhong Tang, Yuting Chen, Ran Li, Jing Yang, Congxin Huang
PURPOSE: Chronically elevated catecholamine levels activate cardiac β-adrenergic receptors, which play a vital role in the pathogenesis of heart failure. Evidence suggests that vasostatin-1 (VS-1) exerts anti-adrenergic effects on isolated and perfused hearts in vitro. Whether VS-1 ameliorates hypertrophy/remodeling by inducing the chronic activation of β-adrenergic receptors is unknown. The present study aims to test the efficacy of using VS-1 to treat the advanced hypertrophy/remodeling that result from chronic β-adrenergic receptor activation and to determine the cellular and molecular mechanisms that underlie this response...
October 2016: Cardiovascular Drugs and Therapy
https://www.readbyqxmd.com/read/27539860/loss-of-myocardial-retinoic-acid-receptor-%C3%AE-induces-diastolic-dysfunction-by-promoting-intracellular-oxidative-stress-and-calcium-mishandling-in-adult-mice
#8
Sen Zhu, Rakeshwar S Guleria, Candice M Thomas, Amanda Roth, Fnu Gerilechaogetu, Rajesh Kumar, David E Dostal, Kenneth M Baker, Jing Pan
Retinoic acid receptor (RAR) has been implicated in pathological stimuli-induced cardiac remodeling. To determine whether the impairment of RARα signaling directly contributes to the development of heart dysfunction and the involved mechanisms, tamoxifen-induced myocardial specific RARα deletion (RARαKO) mice were utilized. Echocardiographic and cardiac catheterization studies showed significant diastolic dysfunction after 16wks of gene deletion. However, no significant differences were observed in left ventricular ejection fraction (LVEF), between RARαKO and wild type (WT) control mice...
October 2016: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/27318036/camkii-dependent-phosphorylation-of-ryr2-promotes-targetable-pathological-ryr2-conformational-shift
#9
Hitoshi Uchinoumi, Yi Yang, Tetsuro Oda, Na Li, Katherina M Alsina, Jose L Puglisi, Ye Chen-Izu, Razvan L Cornea, Xander H T Wehrens, Donald M Bers
Diastolic calcium (Ca) leak via cardiac ryanodine receptors (RyR2) can cause arrhythmias and heart failure (HF). Ca/calmodulin (CaM)-dependent kinase II (CaMKII) is upregulated and more active in HF, promoting RyR2-mediated Ca leak by RyR2-Ser2814 phosphorylation. Here, we tested a mechanistic hypothesis that RyR2 phosphorylation by CaMKII increases Ca leak by promoting a pathological RyR2 conformation with reduced CaM affinity. Acute CaMKII activation in wild-type RyR2, and phosphomimetic RyR2-S2814D (vs. non-phosphorylatable RyR2-S2814A) knock-in mouse myocytes increased SR Ca leak, reduced CaM-RyR2 affinity, and caused a pathological shift in RyR2 conformation (detected via increased access of the RyR2 structural peptide DPc10)...
September 2016: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/27121757/calcium-calmodulin-dependent-kinase-ii-and-nitric-oxide-synthase-1-dependent-modulation-of-ryanodine-receptors-during-%C3%AE-adrenergic-stimulation-is-restricted-to-the-dyadic-cleft
#10
Eef Dries, Demetrio J Santiago, Daniel M Johnson, Guillaume Gilbert, Patricia Holemans, Sanne M Korte, H Llewelyn Roderick, Karin R Sipido
KEY POINTS: The dyadic cleft, where coupled ryanodine receptors (RyRs) reside, is thought to serve as a microdomain for local signalling, as supported by distinct modulation of coupled RyRs dependent on Ca(2+) /calmodulin-dependent kinase II (CaMKII) activation during high-frequency stimulation. Sympathetic stimulation through β-adrenergic receptors activates an integrated signalling cascade, enhancing Ca(2+) cycling and is at least partially mediated through CaMKII. Here we report that CaMKII activation during β-adrenergic signalling is restricted to the dyadic cleft, where it enhances activity of coupled RyRs thereby contributing to the increase in diastolic events...
October 15, 2016: Journal of Physiology
https://www.readbyqxmd.com/read/26542171/calmodulin-kinase-ii-inhibitor-regulates-calcium-homeostasis-changes-caused-by-acute-%C3%AE-adrenergic-receptor-agonist-stimulation-in-mouse-ventricular-myocytes
#11
Yan Huang, Tao Liu, Dandan Wang, Xin Wang, Ran Li, Yuting Chen, Yanhong Tang, Teng Wang, Congxin Huang
Ca(2+)/calmodulin-dependent kinase II (CaMKII) is an important regulatory molecule under chronic β-adrenergic receptor agonist stimulation but cardiac diseases also occur when β-adrenergic elevated acutely in the circulation, of which the most harmful is lethal arrhythmia. The purpose of this study was to explore the effects of acute isoproterenol (ISO) stimulation on intracellular calcium handling and evaluate whether CaMKII inhibitor may change the effects caused by isoproterenol. Mouse ventricular myocytes were acutely isolated by enzymatic method and divided into four groups: control group, ISO group, KN-93 group, ISO + KN-93 group...
February 2016: In Vitro Cellular & Developmental Biology. Animal
https://www.readbyqxmd.com/read/26358004/computational-analysis-of-the-regulation-of-ca-2-dynamics-in-rat-ventricular-myocytes
#12
Scott M Bugenhagen, Daniel A Beard
Force-frequency relationships of isolated cardiac myocytes show complex behaviors that are thought to be specific to both the species and the conditions associated with the experimental preparation. Ca(2+) signaling plays an important role in shaping the force-frequency relationship, and understanding the properties of the force-frequency relationship in vivo requires an understanding of Ca(2+) dynamics under physiologically relevant conditions. Ca(2+) signaling is itself a complicated process that is best understood on a quantitative level via biophysically based computational simulation...
September 11, 2015: Physical Biology
https://www.readbyqxmd.com/read/26297230/small-conductance-ca2-activated-k-current-is-upregulated-via-the-phosphorylation-of-camkii-in-cardiac-hypertrophy-from-spontaneously-hypertensive-rats
#13
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
https://www.readbyqxmd.com/read/26287635/mechanistic-investigation-of-the-arrhythmogenic-role-of-oxidized-camkii-in-the-heart
#14
Panagiota T Foteinou, Joseph L Greenstein, Raimond L Winslow
Oxidative stress and calcium (Ca(2+))/calmodulin (CaM)-dependent protein kinase II (CaMKII) both play important roles in the pathogenesis of cardiac disease. Although the pathophysiological relevance of reactive oxygen species (ROS) and CaMKII has been appreciated for some time, recent work has shown that ROS can directly oxidize CaMKII, leading to its persistent activity and an increase of the likelihood of cellular arrhythmias such as early afterdepolarizations (EADs). Because CaMKII modulates the function of many proteins involved in excitation-contraction coupling, elucidation of its role in cardiac function, in both healthy and oxidative stress conditions, is challenging...
August 18, 2015: Biophysical Journal
https://www.readbyqxmd.com/read/26187182/voltage-gated-sodium-channel-phosphorylation-at-ser571-regulates-late-current-arrhythmia-and-cardiac-function-in-vivo
#15
Patric Glynn, Hassan Musa, Xiangqiong Wu, Sathya D Unudurthi, Sean Little, Lan Qian, Patrick J Wright, Przemyslaw B Radwanski, Sandor Gyorke, Peter J Mohler, Thomas J Hund
BACKGROUND: Voltage-gated Na(+) channels (Nav) are essential for myocyte membrane excitability and cardiac function. Nav current (INa) is a large-amplitude, short-duration spike generated by rapid channel activation followed immediately by inactivation. However, even under normal conditions, a small late component of INa (INa,L) persists because of incomplete/failed inactivation of a subpopulation of channels. Notably, INa,L is directly linked with both congenital and acquired disease states...
August 18, 2015: Circulation
https://www.readbyqxmd.com/read/26147524/the-murine-model-of-mucopolysaccharidosis-iiib-develops-cardiopathies-over-time-leading-to-heart-failure
#16
Gabriele Giacomo Schiattarella, Giuliana Cerulo, Valeria De Pasquale, Pasquale Cocchiaro, Orlando Paciello, Luigi Avallone, Maria Paola Belfiore, Francesca Iacobellis, Daniele Di Napoli, Fabio Magliulo, Cinzia Perrino, Bruno Trimarco, Giovanni Esposito, Paola Di Natale, Luigi Michele Pavone
Mucopolysaccharidosis (MPS) IIIB is a lysosomal disease due to the deficiency of the enzyme α-N-acetylglucosaminidase (NAGLU) required for heparan sulfate (HS) degradation. The disease is characterized by mild somatic features and severe neurological disorders. Very little is known on the cardiac dysfunctions in MPS IIIB. In this study, we used the murine model of MPS IIIB (NAGLU knockout mice, NAGLU(-/-)) in order to investigate the cardiac involvement in the disease. Echocardiographic analysis showed a marked increase in left ventricular (LV) mass, reduced cardiac function and valvular defects in NAGLU(-/-) mice as compared to wild-type (WT) littermates...
2015: PloS One
https://www.readbyqxmd.com/read/26075818/phd2-3-dependent-hydroxylation-tunes-cardiac-response-to-%C3%AE-adrenergic-stress-via-phospholamban
#17
Liang Xie, Xinchun Pi, W H Davin Townley-Tilson, Na Li, Xander H T Wehrens, Mark L Entman, George E Taffet, Ashutosh Mishra, Junmin Peng, Jonathan C Schisler, Gerhard Meissner, Cam Patterson
Ischemic heart disease is the leading cause of heart failure. Both clinical trials and experimental animal studies demonstrate that chronic hypoxia can induce contractile dysfunction even before substantial ventricular damage, implicating a direct role of oxygen in the regulation of cardiac contractile function. Prolyl hydroxylase domain (PHD) proteins are well recognized as oxygen sensors and mediate a wide variety of cellular events by hydroxylating a growing list of protein substrates. Both PHD2 and PHD3 are highly expressed in the heart, yet their functional roles in modulating contractile function remain incompletely understood...
July 1, 2015: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/25896051/-combined-transgenic-inhibition-of-camkii-and-ik1-on-cardiac-remodeling
#18
Yun Huang, Miao Dai, Yi-Mei Du, Yu-Feng Yao, Jia-Ming Zhang, Guan-Hua Su, Yan-Wen Shu, Tian-Pen Cui, Xin-Ling Du, Jing-Dong Li
This study was aimed to establish an experimental mouse model of combined transgenic inhibition of both multifunctional Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) and inward rectifier potassium current (Ik1), and to observe whether the specific inhibition of both CaMKII and Ik1 can bring about any effects on cardiac remodeling. Mice were divided into 4 groups: wild type (WT), CaMKII inhibited (AC3-I), Ik1 inhibited (Kir2.1-AAA) and combined inhibition of both CaMKII and Ik1 (AC3-I+Kir2.1-AAA). Mice in each group received electrocardiogram (ECG) and echocardiography examination...
April 25, 2015: Sheng Li Xue Bao: [Acta Physiologica Sinica]
https://www.readbyqxmd.com/read/25887954/%C3%AE-%C3%A2-adrenoceptor-stimulation-promotes-lps-induced-cardiomyocyte-apoptosis-through-activating-pka-and-enhancing-camkii-and-i%C3%AE%C2%BAb%C3%AE-phosphorylation
#19
Yiyang Wang, Yuan Wang, Duomeng Yang, Xiaohui Yu, Hongmei Li, Xiuxiu Lv, Daxiang Lu, Huadong Wang
INTRODUCTION: Caspase activation and cardiomyocyte apoptosis have been implicated in lipopolysaccharide (LPS)-induced cardiac contractile dysfunction. We have recently demonstrated that β1-adrenoceptor (AR) activation by endogenous norepinephrine contributes to cardiomyocyte apoptosis in endotoxemic mice. Here, we further investigated the molecular mechanisms for the enhancing effect of β₁-AR activation on LPS-induced cardiomyocyte apoptosis. METHODS: The adult mouse ventricular myocytes were exposed to LPS, dobutamine, protein kinase A (PKA) inhibitor or/and nifedipine, an L-type Ca(2+) channel blocker...
2015: Critical Care: the Official Journal of the Critical Care Forum
https://www.readbyqxmd.com/read/25820375/nuclear-translocation-of-calpain-2-mediates-apoptosis-of-hypertrophied-cardiomyocytes-in-transverse-aortic-constriction-rat
#20
Juan-Juan Sheng, Hui Chang, Zhi-Bin Yu
Apoptosis of cardiomyocytes plays an important role in the transition from cardiac hypertrophy to heart failure. Hypertrophied cardiomyocytes show enhanced susceptibility to apoptosis. Therefore, the aim of this study was to determine the susceptibility to apoptosis and its mechanism in hypertrophied cardiomyocytes using a rat model of transverse abdominal aortic constriction (TAC). Sixteen weeks of TAC showed compensatory and pathological hypertrophy in the left ventricle. TUNEL-positive nuclei were significantly increased in TAC with angiotensin II (Ang II) treatment...
November 2015: Journal of Cellular Physiology
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