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Cardiac Contractility Modulation

Nourdine Chakouri, Cyril Reboul, Doria Boulghobra, Adrien Kleindienst, Stéphane Nottin, Sandrine Gayrard, François Roubille, Stefan Matecki, Alain Lacampagne, Olivier Cazorla
BACKGROUND: The interplay between oxidative stress and other signaling pathways in the contractile machinery regulation during cardiac stress and its consequences on cardiac function remains poorly understood. We evaluated the effect of the crosstalk between β-adrenergic and redox signaling on post-translational modifications of sarcomeric regulatory proteins, Myosin Binding Protein-C (MyBP-C) and Troponin I (TnI). METHODS AND RESULTS: We mimicked in vitro high level of physiological cardiac stress by forcing rat hearts to produce high levels of oxidized glutathione...
May 1, 2018: International Journal of Cardiology
Ni Zhu, Bing Yi, Zhifu Guo, Guanxin Zhang, Shengdong Huang, Yongwen Qin, Xianxian Zhao, Jianxin Sun
BACKGROUND/AIMS: Pim-1 is a serine/threonine kinase that is highly expressed in the heart, and exerts potent cardiac protective effects through enhancing survival, proliferation, and regeneration of cardiomyocytes. Its myocardial specific substrates, however, remain unknown. In the present study, we aim to investigate whether Pim-1 modulates myofilament activity through phosphorylation of cardiac troponin I (cTnI), a key component in regulating myofilament function in the heart. METHODS: Coimmunoprecipitation and immunofluorescent assays were employed to investigate the interaction of Pim-1 with cTnI in cardiomyocytes...
March 10, 2018: Cellular Physiology and Biochemistry
Gary C H Gan, Aaisha Ferkh, Anita Boyd, Liza Thomas
The left atrium has an important role in modulating left ventricular filling and is an important biomarker of cardiovascular disease and adverse cardiovascular outcomes. While previously left atrial (LA) size was utilised, the role of LA function as a biomarker is increasingly being evaluated, both independently and also in combination with LA size. Strain analysis has been utilised for evaluation of LA function and can be measured throughout the cardiac cycle, thereby enabling the evaluation of LA reservoir, conduit and contractile function...
February 2018: Cardiovascular Diagnosis and Therapy
Petra Bilić, Nicolas Guillemin, Alan Kovačević, Blanka Beer Ljubić, Ines Jović, Asier Galan, Peter David Eckersall, Richard Burchmore, Vladimir Mrljak
Idiopathic dilated cardiomyopathy (iDCM) is a primary myocardial disorder with an unknown aetiology, characterized by reduced contractility and ventricular dilation of the left or both ventricles. Naturally occurring canine iDCM was used herein to identify serum proteomic signature of the disease compared to the healthy state, providing an insight into underlying mechanisms and revealing proteins with biomarker potential. To achieve this, we used high-throughput label-based quantitative LC-MS/MS proteomics approach and bioinformatics analysis of the in silico inferred interactome protein network created from the initial list of differential proteins...
March 9, 2018: Journal of Proteomics
Rebeca Caldeira Machado Berger, Acaris Benetti, Adriana Castello Costa Girardi, Ludimila Forechi, Rafaella Martins de Oliveira, Paula Frizera Vassallo, José Geraldo Mill
BACKGROUND: High sodium intake contributes to the pathogenesis of hypertension and adversely affects cardiac function. Conversely, sodium reduction is associated with a blood pressure decrease and improved cardiovascular function. However, the mechanisms that underlie the cardiac effects induced by salt intake in hypertension have not been fully elucidated. Ca2+ handling is critical for efficient myocardial function; thus, we aimed to investigate the long-term effects of diets with different salt contents on cardiac function and Ca2+ handling proteins in spontaneously hypertensive rats (SHRs)...
March 5, 2018: American Journal of Hypertension
Stanley M Walls, Anthony Cammarato, Dale A Chatfield, Karen Ocorr, Greg L Harris, Rolf Bodmer
Lipotoxic cardiomyopathy (LCM) is characterized by abnormal myocardial accumulation of lipids, including ceramide; however, the contribution of ceramide to the etiology of LCM is unclear. Here, we investigated the association of ceramide metabolism and ceramide-interacting proteins (CIPs) in LCM in the Drosophila heart model. We find that ceramide feeding or ceramide-elevating genetic manipulations are strongly associated with cardiac dilation and defects in contractility. High ceramide-associated LCM is prevented by inhibiting ceramide synthesis, establishing a robust model of direct ceramide-associated LCM, corroborating previous indirect evidence in mammals...
March 6, 2018: Cell Reports
Ioannis Smyrnias, Normann Goodwin, Dagmar Wachten, Jonas Skogestad, Jan Magnus Aronsen, Emma L Robinson, Kateryna Demydenko, Anne Segonds-Pichon, David Oxley, Sakthivel Sadayappan, Karin Sipido, Martin D Bootman, H Llewelyn Roderick
The shortening of sarcomeres that co-ordinates the pump function of the heart is stimulated by electrically-mediated increases in [Ca2+ ]. This process of excitation-contraction coupling (ECC) is subject to modulation by neurohormonal mediators that tune the output of the heart to meet the needs of the organism. Endothelin-1 (ET-1) is a potent modulator of cardiac function with effects on contraction amplitude, chronotropy and automaticity. The actions of ET-1 are evident during normal adaptive physiological responses and increased under pathophysiological conditions, such as following myocardial infarction and during heart failure, where ET-1 levels are elevated...
February 19, 2018: Journal of Molecular and Cellular Cardiology
Thassio R Mesquita, Gaelle Auguste, Debora Falcón, Gema Ruiz-Hurtado, Rogelio Salazar-Enciso, Jessica Sabourin, Florence Lefebvre, Say Viengchareun, Hussein Kobeissy, Patrick Lechêne, Valerie Nicolas, Amaya Fernández-Celis, Susana Gomez, Sandra Lauton-Santos, Eric Morel, Angelica Rueda, Natalia López-Andrés, Ana M Gomez, Marc Lombes, Jean-Pierre Benitah
<u>Rationale:</u> The mineralocorticoid receptor (MR) antagonists belong to the current therapeutic armamentarium for the management of cardiovascular diseases, but the mechanisms conferring their beneficial effects are poorly understood. Part of the cardiovascular effects of MR are due to the regulation of L-type Cav 1.2 Ca2+ channel expression, which is generated by tissue-specific alternative promoters as a long 'cardiac' (Cav 1.2-LNT) or a short 'vascular' (Cav 1.2-SNT) N-terminal transcripts...
February 21, 2018: Circulation Research
Refaat A Eid, Mahmoud A Alkhateeb, Mubarak Al-Shraim, Samy M Eleawa, Abdullah S Shatoor, Attalla Farag El-Kott, Mohamed Samir Ahmed Zaki, Khalid A Shatoor, Ismaeel Bin-Jaliah, Fahaid H Al-Hashem
CONTEXT: Mechanisms by which ghrelin affords its cardioprotection in mammals remained unclear. OBJECTIVE: To examine if ghrelin confers cardio-protection during cardiac remodelling post-MI by modulating the RAF-1-MEK1/2-ERK1/2 signalling pathway. MATERIALS AND METHODS: Rats were divided into control, sham, sham + ghrelin, myocardial infarction (MI), and MI + ghrelin groups. Ghrelin (100 µg/kg) was administered for 21 days, starting one-day post-MI...
February 15, 2018: Archives of Physiology and Biochemistry
Heloise Mongue-Din, Ashish S Patel, Yee H Looi, David J Grieve, Narayana Anilkumar, Alexander Sirker, Xuebin Dong, Alison C Brewer, Min Zhang, Alberto Smith, Ajay M Shah
The reactive oxygen species-generating enzyme NADPH oxidase 4 (Nox4) is up-regulated in the heart after myocardial infarction (MI). Mice with cardiomyocyte-targeted Nox4 overexpression (TG) displayed increased macrophages in the heart at baseline, with skewing toward an M2 phenotype compared with wild-type controls (WT). After MI, TG mice had a higher proportion of M2 macrophages along with higher survival, decreased cardiac remodeling, and better contractile function than wild-type mice. The post-MI increase in cardiac matrix metalloproteinase-2 activity was substantially blunted in TG mice...
December 2017: JACC. Basic to Translational Science
Zhong Chen, Na Xu, Danyang Chong, Shan Guan, Chen Jiang, Zhongzhou Yang, Chaojun Li
Aims: With the maturation of placenta, ventricular chamber maturation enhances cardiac contractile performance to adapt to the metabolic demand of growing embryo. The organization of cardiomyocytes is required for the morphological remodeling in ventricular chamber maturation. However, the mechanism governing the establishment of cardiac cytoarchitecture during ventricular chamber maturation is still poorly studied. Methods and results: Here, we found that the expression of geranylgeranyl pyrophosphate synthase (Ggpps), which mediates protein geranylgeranylation, increased in the mouse heart after the onset of placental function...
February 12, 2018: Cardiovascular Research
Lei Yao, Duanyang Xie, Li Geng, Dan Shi, Jian Huang, Yufei Wu, Fei Lv, Dandan Liang, Li Li, Yi Liu, Jun Li, Yi-Han Chen
BACKGROUND: Heart failure is a complex syndrome characterized by cardiac contractile impairment with high mortality. Defective intracellular Ca2+ homeostasis is the central cause under this scenario and tightly links to ultrastructural rearrangements of sarcolemmal transverse tubules and the sarcoplasmic reticulum (SR); however, the modulators of the SR architecture remain unknown. The SR has been thought to be a specialized endoplasmic reticulum membrane system. Receptor accessory proteins (REEPs)/DP1/Yop1p are responsible for shaping high-curvature endoplasmic reticulum tubules...
February 3, 2018: Journal of the American Heart Association
Matthew Movsesian, Faiyaz Ahmad, Emilio Hirsch
Isoforms in the PDE3 family of cyclic nucleotide phosphodiesterases have important roles in cyclic nucleotide-mediated signalling in cardiac myocytes. These enzymes are targeted by inhibitors used to increase contractility in patients with heart failure, with a combination of beneficial and adverse effects on clinical outcomes. This review covers relevant aspects of the molecular biology of the isoforms that have been identified in cardiac myocytes; the roles of these enzymes in modulating cAMP-mediated signalling and the processes mediated thereby; and the potential for targeting these enzymes to improve the profile of clinical responses...
February 6, 2018: Journal of Cardiovascular Development and Disease
Lin Wang, Nanhu Quan, Wanqing Sun, Xu Chen, Courtney Cates, Thomas Rousselle, Xinchun Zhou, Xuezhong Zhao, Ji Li
Aim: A longevity gene, Sirtuin 1 (SIRT1) and energy sensor AMP-activated protein kinase (AMPK) have common activators such as caloric restriction, oxidative stress and exercise. The objective of this study is to characterize the role of cardiomyocyte SIRT1 in age-related impaired ischemic AMPK activation and increased susceptibility to ischemic insults. Methods and Results: Mice were subjected to ligation of left anterior descending coronary artery for in vivo ischemic models...
February 2, 2018: Cardiovascular Research
Viviana Meraviglia, Leonardo Bocchi, Roberta Sacchetto, Maria Cristina Florio, Benedetta M Motta, Corrado Corti, Christian X Weichenberger, Monia Savi, Yuri D'Elia, Marcelo D Rosato-Siri, Silvia Suffredini, Chiara Piubelli, Giulio Pompilio, Peter P Pramstaller, Francisco S Domingues, Donatella Stilli, Alessandra Rossini
SERCA2a is the Ca2+ ATPase playing the major contribution in cardiomyocyte (CM) calcium removal. Its activity can be regulated by both modulatory proteins and several post-translational modifications. The aim of the present work was to investigate whether the function of SERCA2 can be modulated by treating CMs with the histone deacetylase (HDAC) inhibitor suberanilohydroxamic acid (SAHA). The incubation with SAHA (2.5 µM, 90 min) of CMs isolated from rat adult hearts resulted in an increase of SERCA2 acetylation level and improved ATPase activity...
January 31, 2018: International Journal of Molecular Sciences
Gabriel Camargo-Silva, Larissa Córdova Turones, Kellen Rosa da Cruz, Karina Pereira Gomes, Michelle Mendanha Mendonça, Allancer Nunes, Itamar Guedes de Jesus, Diego Basile Colugnati, Aline Priscila Pansani, Roger Luis Henschel Pobbe, Robson Santos, Marco Antônio Peliky Fontes, Silvia Guatimosim, Carlos Henrique de Castro, Danielle Ianzer, Reginaldo Nassar Ferreira, Carlos Henrique Xavier
Prior evidence indicates that ghrelin is involved in the integration of cardiovascular functions and behavioral responses. Ghrelin actions are mediated by the growth hormone secretagogue receptor subtype 1a (GHS-R1a), which is expressed in peripheral tissues and central areas involved in the control of cardiovascular responses to stress. AIMS: In the present study, we assessed the role of ghrelin - GHS-R1a axis in the cardiovascular reactivity to acute emotional stress in rats. MAIN METHODS AND KEY FINDINGS: Ghrelin potentiated the tachycardia evoked by restraint and air jet stresses, which was reverted by GHS-R1a blockade...
January 20, 2018: Life Sciences
Yun-Ping Mu, Qiu-Hong Huang, Jie-Ling Zhu, Si-Yi Zheng, Fu-Rong Yan, Xiao-Ling Zhuang, James S K Sham, Mo-Jun Lin
Pulmonary hypertension (PH) is characterized by enhanced vasoreactivity and sustained pulmonary vasoconstriction, arising from the aberrant Ca2+ homeostasis in pulmonary arterial smooth muscle cells. In addition to Ca2+ , magnesium, the most abundant intracellular divalent cation, also plays critical roles in many cellular processes that regulate cardiovascular functions. Recent findings suggested that magnesium regulates vascular functions by altering the vascular responses to vasodilator and vasoactive agonists, and affects endothelial function by modulating endothelium-dependent vasodilation in hypertension...
January 23, 2018: Experimental Physiology
Koji Yoshie, Pradeep S Rajendran, Louis Massoud, OhJin Kwon, Vasudev Tadimeti, Siamak Salavatian, Jeffrey Laurence Ardell, Kalyanam Shivkumar, Olujimi A Ajijola
Afferent fibers expressing the vanilloid receptor 1 (VR1) channel are implicated in cardiac nociception, however, their role in modulating reflex responses to cardiac stress is not well-understood. We evaluated this role in Yorkshire pigs by percutaneous epicardial application of resiniferatoxin (RTX), a toxic activator of the VR1 channel, resulting in depletion of cardiac VR1-expressing afferents. Hemodynamics, epicardial activation recovery intervals (ARIs), and in vivo activity of stellate ganglion (SG) neurons (SGNs) were recorded in control and RTX-treated animals...
January 16, 2018: American Journal of Physiology. Heart and Circulatory Physiology
D M Schwab, L Tilemann, R Bauer, M Heckmann, A Jungmann, M Wagner, J Burgis, C Vettel, H A Katus, A El-Armouche, O J Müller
The downregulation of β-adrenergic receptors (β-AR) and decreased cAMP-dependent protein kinase activity in failing hearts results in decreased phosphorylation and inactivation of phosphatase-inhibitor-1 (I-1), a distal amplifier element of β-adrenergic signaling, leading to increased protein phosphatase 1 activity and dephosphorylation of key phosphoproteins, including phospholamban. Downregulated and hypophosphorylated I-1 likely contributes to β-AR desensitization; therefore its modulation is a promising approach in heart failure treatment...
January 2018: Gene Therapy
Scott John, Brian Kim, Riccardo Olcese, Joshua I Goldhaber, Michela Ottolia
The cardiac Na+-Ca2+ exchanger (NCX) plays a critical role in the heart by extruding Ca2+ after each contraction and thus regulates cardiac contractility. The activity of NCX is strongly inhibited by cytosolic protons, which suggests that intracellular acidification will have important effects on heart contractility. However, the mechanisms underlying this inhibition remain elusive. It has been suggested that pH regulation originates from the competitive binding of protons to two Ca2+-binding domains within the large cytoplasmic loop of NCX and requires inactivation by intracellular Na+ to fully develop...
January 4, 2018: Journal of General Physiology
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