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Cardiac Calcium/calmodulin-dependent kinase type II

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https://www.readbyqxmd.com/read/29650543/rbm20-mutations-induce-an-arrhythmogenic-dilated-cardiomyopathy-related-to-disturbed-calcium-handling
#1
Maarten M G van den Hoogenhof, Abdelaziz Beqqali, Ahmad S Amin, Ingeborg van der Made, Simona Aufiero, Mohsin A F Khan, Cees A Schumacher, Joeri A Jansweijer, Karin Y van Spaendonck-Zwarts, Carol Ann Remme, Johannes Backs, Arie O Verkerk, Antonius Baartscheer, Yigal M Pinto, Esther E Creemers
Background -Mutations in RBM20 cause a clinically aggressive form of dilated cardiomyopathy (DCM), with an increased risk of malignant ventricular arrhythmias. RBM20 is a splicing factor that targets multiple pivotal cardiac genes, such as Titin (TTN) and Calcium/calmodulin-dependent kinase II delta (CAMK2D). Aberrant TTN splicing is thought to be the main determinant of RBM20-induced DCM, but is not likely to explain the increased risk of arrhythmias. Here, we investigated the extent at which RBM20 mutation carriers have an increased risk of arrhythmias and explore the underlying molecular mechanism...
April 12, 2018: Circulation
https://www.readbyqxmd.com/read/29409723/camkii-in-vascular-signalling-friend-or-foe
#2
REVIEW
Obialunanma V Ebenebe, Alison Heather, Jeffrey R Erickson
Signalling mechanisms within and between cells of the vasculature enable function and maintain homeostasis. However, a number of these mechanisms also contribute to the pathophysiology of vascular disease states. The multifunctional signalling molecule calcium/calmodulin-dependent kinase II (CaMKII) has been shown to have critical functional effects in many tissue types. For example, CaMKII is known to have a dual role in cardiac physiology and pathology. The function of CaMKII within the vasculature is incompletely understood, but emerging evidence points to potential physiological and pathological roles...
May 2018: Heart, Lung & Circulation
https://www.readbyqxmd.com/read/28855948/astragalus-granule-prevents-ca-2-current-remodeling-in-heart-failure-by-the-downregulation-of-camkii
#3
Sinai Li, Yibing Nong, Qun Gao, Jing Liu, Yan Li, Xiaoyun Cui, Jie Wan, Jinjin Lu, Mingjie Sun, Qian Wu, Xiaolu Shi, Haifeng Cui, Weihong Liu, Mingxue Zhou, Lina Li, Qian Lin
BACKGROUND: Astragalus was broadly used for treating heart failure (HF) and arrhythmias in East Asia for thousands of years. Astragalus granule (AG), extracted from Astragalus, shows beneficial effect on the treatment of HF in clinical research. We hypothesized that administration of AG prevents the remodeling of L-type Ca(2+) current (ICa-L) in HF mice by the downregulation of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII). METHODS: HF mice were induced by thoracic aortic constriction (TAC)...
2017: Evidence-based Complementary and Alternative Medicine: ECAM
https://www.readbyqxmd.com/read/28842915/roles-of-impaired-intracellular-calcium-cycling-in-arrhythmogenicity-of-diabetic-mouse-model
#4
Chung-Chuan Chou, Chien-Te Ho, Hui-Ling Lee, Yen Chu, Tzung-Hai Yen, Ming-Shien Wen, Shien-Fong Lin, Cheng-Hung Lee, Po-Cheng Chang
BACKGROUND: Diabetes mellitus is associated an increased risk of ventricular arrhythmias (VAs), but the underlying electrophysiological mechanisms are not fully explored. This study was aimed to test whether dynamic factors and Cai handling play roles in arrhythmogenesis of a diabetic animal model. METHODS: We used 26 db/db type 2 diabetes mice and 28 control mice in this study. VA inducibility was evaluated in vivo under isoflurane general anesthesia. The intracellular Ca(2+) (Cai ) and membrane voltage (Vm ) signals of the Langendorff-perfused mouse hearts were simultaneously recorded using the optical mapping technique...
August 26, 2017: Pacing and Clinical Electrophysiology: PACE
https://www.readbyqxmd.com/read/28573136/effects-of-wenxin-keli-on-cardiac-hypertrophy-and-arrhythmia-via-regulation-of-the-calcium-calmodulin-dependent-kinase-ii-signaling-pathway
#5
Xinyu Yang, Yu Chen, Yanda Li, Xiaomeng Ren, Yanwei Xing, Hongcai Shang
We investigated the effects of Wenxin Keli (WXKL) on the Calcium/Calmodulin dependent kinase II (CaMK II) signal transduction pathway with transverse aortic constriction (TAC) rats. Echocardiographic measurements were obtained 3 and 9 weeks after the surgery. Meanwhile, the action potentials (APDs) were recorded using the whole-cell patch clamp technique, and western blotting was used to assess components of the CaMK II signal transduction pathway. At both 3 and 9 weeks after treatment, the fractional shortening (FS%) increased in the WXKL group compared with the TAC group...
2017: BioMed Research International
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
#6
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
#7
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
#8
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
#9
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
#10
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
#11
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
#12
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
#13
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
#14
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
#15
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 Ca2+ /calmodulin-dependent kinase II (CaMKII) activation during high-frequency stimulation. Sympathetic stimulation through β-adrenergic receptors activates an integrated signalling cascade, enhancing Ca2+ 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
#16
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
#17
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
#18
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
#19
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
#20
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
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