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1. p38γ/δ activation alters cardiac electrical activity and predisposes to ventricular arrhythmia

Author

Romero-Becerra, Rafael, Cruz, Francisco M., Mora, Alfonso, Lopez, Juan Antonio, Ponce-Balbuena, Daniela, Allan, Andrew, Ramos-Mondragón, Roberto, González-Terán, Bárbara, León, Marta, Rodríguez, Maria Elena, Leiva-Vega, Luis, Guerrero-Serna, Guadalupe, Jimenez-Vazquez, Eric N., Filgueiras-Rama, David, Vázquez, Jesús, Jalife, José, and Sabio, Guadalupe

Published
2023
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5. ABCC9 is a novel Brugada and early repolarization syndrome susceptibility gene.

Author

Hu, Dan, Barajas-Martínez, Hector, Terzic, Andre, Park, Sungjo, Pfeiffer, Ryan, Burashnikov, Elena, Wu, Yuesheng, Borggrefe, Martin, Veltmann, Christian, Schimpf, Rainer, Cai, John, Nam, Gi-Byong, Deshmukh, Pramod, Preminger, Mark, Steinberg, Jonathan, López-Izquierdo, Angélica, Ponce-Balbuena, Daniela, Wolpert, Christian, Haïssaguerre, Michel, Sánchez-Chapula, José, Antzelevitch, Charles, and Scheinman, Melvin

Subjects
ATP-sensitive potassium channel, J wave syndromes, Mutation, Sodium channel, Sudden cardiac death, Adolescent, Adult, Aged, Amino Acid Sequence, Animals, Brugada Syndrome, Female, Genetic Predisposition to Disease, HEK293 Cells, Humans, Male, Mice, Middle Aged, Molecular Sequence Data, Mutation, Protein Structure, Secondary, Rabbits, Rats, Sulfonylurea Receptors, Young Adult
Abstract

BACKGROUND: Genetic defects in KCNJ8, encoding the Kir6.1 subunit of the ATP-sensitive K(+) channel (I(K-ATP)), have previously been associated with early repolarization (ERS) and Brugada (BrS) syndromes. Here we test the hypothesis that genetic variants in ABCC9, encoding the ATP-binding cassette transporter of IK-ATP (SUR2A), are also associated with both BrS and ERS. METHODS AND RESULTS: Direct sequencing of all ERS/BrS susceptibility genes was performed on 150 probands and family members. Whole-cell and inside-out patch-clamp methods were used to characterize mutant channels expressed in TSA201-cells. Eight ABCC9 mutations were uncovered in 11 male BrS probands. Four probands, diagnosed with ERS, carried a highly-conserved mutation, V734I-ABCC9. Functional expression of the V734I variant yielded a Mg-ATP IC₅₀ that was 5-fold that of wild-type (WT). An 18-y/o male with global ERS inherited an SCN5A-E1784K mutation from his mother, who displayed long QT intervals, and S1402C-ABCC9 mutation from his father, who displayed an ER pattern. ABCC9-S1402C likewise caused a gain of function of IK-ATP with a shift of ATP IC₅₀ from 8.5 ± 2 mM to 13.4 ± 5 μM (p

Published
2014

7. Tbx20 controls the expression of the KCNH2 gene and of hERG channels

Author

Caballero, Ricardo, Utrilla, Raquel G., Amorós, Irene, Matamoros, Marcos, Pérez-Hernández, Marta, Tinaquero, David, Alfayate, Silvia, Nieto-Marín, Paloma, Guerrero-Serna, Guadalupe, Liu, Qing-hua, Ramos-Mondragón, Roberto, Ponce-Balbuena, Daniela, Herron, Todd, Campbell, Katherine F., Filgueiras-Rama, David, Peinado, Rafael, López-Sendón, José L., Jalife, José, Delpón, Eva, and Tamargo, Juan

Published
2017

8. Galectin-3 Regulates Atrial Fibrillation Remodeling and Predicts Catheter Ablation Outcomes

Author

Takemoto, Yoshio, Ramirez, Rafael J., Yokokawa, Miki, Kaur, Kuljeet, Ponce-Balbuena, Daniela, Sinno, Mohamad C., Willis, B. Cicero, Ghanbari, Hamid, Ennis, Steven R., Guerrero-Serna, Guadalupe, Henzi, Bettina C., Latchamsetty, Rakesh, Ramos-Mondragon, Roberto, Musa, Hassan, Martins, Raphael P., Pandit, Sandeep V., Noujaim, Sami F., Crawford, Thomas, Jongnarangsin, Krit, Pelosi, Frank, Bogun, Frank, Chugh, Aman, Berenfeld, Omer, Morady, Fred, Oral, Hakan, and Jalife, José

Published
2016
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9. Cardiac Kir2.1 and NaV1.5 Channels Traffic Together to the Sarcolemma to Control Excitability

Author

Ponce-Balbuena, Daniela, Guerrero-Serna, Guadalupe, Valdivia, Carmen R., Caballero, Ricardo, Diez-Guerra, F. Javier, Jiménez-Vázquez, Eric N., Ramírez, Rafael J., Monteiro da Rocha, André, Herron, Todd J., Campbell, Katherine F., Willis, B. Cicero, Alvarado, Francisco J., Zarzoso, Manuel, Kaur, Kuljeet, Pérez-Hernández, Marta, Matamoros, Marcos, Valdivia, Héctor H., Delpón, Eva, and Jalife, José

Published
2018
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10. SNTA1 gene rescues ion channel function and is antiarrhythmic in cardiomyocytes derived from induced pluripotent stem cells from muscular dystrophy patients

Author

Jimenez-Vazquez, Eric N, primary, Arad, Michael, additional, Macías, Álvaro, additional, Vera-Pedrosa, Maria L, additional, Cruz, Francisco Miguel, additional, Gutierrez, Lilian K, additional, Cuttita, Ashley J, additional, Monteiro da Rocha, André, additional, Herron, Todd J, additional, Ponce-Balbuena, Daniela, additional, Guerrero-Serna, Guadalupe, additional, Binah, Ofer, additional, Michele, Daniel E, additional, and Jalife, José, additional

Published
2022
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11. Author response: SNTA1 gene rescues ion channel function and is antiarrhythmic in cardiomyocytes derived from induced pluripotent stem cells from muscular dystrophy patients

Author

Jimenez-Vazquez, Eric N, primary, Arad, Michael, additional, Macías, Álvaro, additional, Vera-Pedrosa, Maria L, additional, Cruz, Francisco Miguel, additional, Gutierrez, Lilian K, additional, Cuttita, Ashley J, additional, Monteiro da Rocha, André, additional, Herron, Todd J, additional, Ponce-Balbuena, Daniela, additional, Guerrero-Serna, Guadalupe, additional, Binah, Ofer, additional, Michele, Daniel E, additional, and Jalife, José, additional

Published
2022
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12. SNTA1 GeneRescues Ion Channel Function in Cardiomyocytes Derived from Induced Pluripotent Stem Cells Reprogrammed from Muscular Dystrophy Patients with Arrhythmias

Author

Jalife, José, primary, Jimenez-Vazquez, Eric N, additional, Arad, Michael, additional, Macías, Álvaro, additional, Vera-Pedrosa, Maria L, additional, Cruz, Francisco Miguel, additional, Cuttita, Ashley J, additional, Monteiro da Rocha, André, additional, Herron, Todd J, additional, Ponce-Balbuena, Daniela, additional, Guerrero-Serna, Guadalupe, additional, Binah, Ofer, additional, and Michele, Daniel E, additional

Published
2022
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15. In vitro model of ischemic heart failure using human induced pluripotent stem cell–derived cardiomyocytes

Author

Davis, Justin, primary, Chouman, Ahmad, additional, Creech, Jeffery, additional, Monteiro da Rocha, Andre, additional, Ponce-Balbuena, Daniela, additional, Jimenez Vazquez, Eric N., additional, Nichols, Ruthann, additional, Lozhkin, Andrey, additional, Madamanchi, Nageswara R., additional, Campbell, Katherine F., additional, and Herron, Todd J., additional

Published
2021
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17. Paclitaxel mitigates structural alterations and cardiac conduction system defects in a mouse model of Hutchinson–Gilford progeria syndrome

Author

Macías, Álvaro, primary, Díaz-Larrosa, J Jaime, additional, Blanco, Yaazan, additional, Fanjul, Víctor, additional, González-Gómez, Cristina, additional, Gonzalo, Pilar, additional, Andrés-Manzano, María Jesús, additional, da Rocha, Andre Monteiro, additional, Ponce-Balbuena, Daniela, additional, Allan, Andrew, additional, Filgueiras-Rama, David, additional, Jalife, José, additional, and Andrés, Vicente, additional

Published
2021
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18. Paclitaxel mitigates structural alterations and cardiac conduction system defects in a mouse model of Hutchinson–Gilford progeria syndrome.

Author

Macías, Álvaro, Díaz-Larrosa, J Jaime, Blanco, Yaazan, Fanjul, Víctor, González-Gómez, Cristina, Gonzalo, Pilar, Andrés-Manzano, María Jesús, Rocha, Andre Monteiro da, Ponce-Balbuena, Daniela, Allan, Andrew, Filgueiras-Rama, David, Jalife, José, and Andrés, Vicente

Subjects
HEART conduction system, PROGERIA, PACLITAXEL, HEART beat, LABORATORY mice
Abstract

Aims Hutchinson–Gilford progeria syndrome (HGPS) is an ultrarare laminopathy caused by expression of progerin, a lamin A variant, also present at low levels in non-HGPS individuals. HGPS patients age and die prematurely, predominantly from cardiovascular complications. Progerin-induced cardiac repolarization defects have been described previously, although the underlying mechanisms are unknown. Methods and results We conducted studies in heart tissue from progerin-expressing LmnaG609G/G609G (G609G) mice, including microscopy, intracellular calcium dynamics, patch-clamping, in vivo magnetic resonance imaging, and electrocardiography. G609G mouse cardiomyocytes showed tubulin-cytoskeleton disorganization, t-tubular system disruption, sarcomere shortening, altered excitation–contraction coupling, and reductions in ventricular thickening and cardiac index. G609G mice exhibited severe bradycardia, and significant alterations of atrio-ventricular conduction and repolarization. Most importantly, 50% of G609G mice had altered heart rate variability, and sinoatrial block, both significant signs of premature cardiac aging. G609G cardiomyocytes had electrophysiological alterations, which resulted in an elevated action potential plateau and early afterdepolarization bursting, reflecting slower sodium current inactivation and long Ca+2 transient duration, which may also help explain the mild QT prolongation in some HGPS patients. Chronic treatment with low-dose paclitaxel ameliorated structural and functional alterations in G609G hearts. Conclusions Our results demonstrate that tubulin-cytoskeleton disorganization in progerin-expressing cardiomyocytes causes structural, cardiac conduction, and excitation–contraction coupling defects, all of which can be partially corrected by chronic treatment with low dose paclitaxel. [ABSTRACT FROM AUTHOR]

Published
2022
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21. Kir2.1 Interactome Mapping Uncovers PKP4 as a Modulator of the Kir2.1-Regulated Inward Rectifier Potassium Currents

Author

Park, Sung-Soo, primary, Ponce-Balbuena, Daniela, additional, Kuick, Rork, additional, Guerrero-Serna, Guadalupe, additional, Yoon, Justin, additional, Mellacheruvu, Dattatreya, additional, Conlon, Kevin P., additional, Basrur, Venkatesha, additional, Nesvizhskii, Alexey I., additional, Jalife, José, additional, and Rual, Jean-François, additional

Published
2020
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22. Human influenza A virus causes myocardial and cardiac-specific conduction system infections associated with early inflammation and premature death

Author

Filgueiras-Rama, David, primary, Vasilijevic, Jasmina, additional, Jalife, Jose, additional, Noujaim, Sami F, additional, Alfonso, Jose M, additional, Nicolas-Avila, Jose A, additional, Gutierrez, Celia, additional, Zamarreño, Noelia, additional, Hidalgo, Andres, additional, Bernabé, Alejandro, additional, Cop, Christopher Pablo, additional, Ponce-Balbuena, Daniela, additional, Guerrero-Serna, Guadalupe, additional, Calle, Daniel, additional, Desco, Manuel, additional, Ruiz-Cabello, Jesus, additional, Nieto, Amelia, additional, and Falcon, Ana, additional

Published
2020
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23. Brugada syndrome trafficking-defective Nav1.5 channels can trap cardiac Kir2.1/2.2 channels

Author

Pérez-Hernández, Marta, Matamoros, Marcos, Alfayate, Silvia, Nieto-Marín, Paloma, Utrilla, Raquel G, Tinaquero, David, de Andrés, Raquel, Crespo, Teresa, Ponce-Balbuena, Daniela, Willis, B Cicero, Jiménez-Vazquez, Eric N, Guerrero-Serna, Guadalupe, da Rocha, Andre M, Campbell, Katherine, Herron, Todd J, Díez-Guerra, F Javier, Tamargo, Juan, Jalife, José, Caballero, Ricardo, and Delpón, Eva

Subjects
cardiovascular system, Cardiology, Sodium channels, Cell Biology, Arrhythmias, Potassium channels
Abstract

Cardiac Nav1.5 and Kir2.1-2.3 channels generate Na (INa) and inward rectifier K (IK1) currents, respectively. The functional INa and IK1 interplay is reinforced by the positive and reciprocal modulation between Nav15 and Kir2.1/2.2 channels to strengthen the control of ventricular excitability. Loss-of-function mutations in the SCN5A gene, which encodes Nav1.5 channels, underlie several inherited arrhythmogenic syndromes, including Brugada syndrome (BrS). We investigated whether the presence of BrS-associated mutations alters IK1 density concomitantly with INa density. Results obtained using mouse models of SCN5A haploinsufficiency, and the overexpression of native and mutated Nav1.5 channels in expression systems - rat ventricular cardiomyocytes and human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) - demonstrated that endoplasmic reticulum (ER) trafficking-defective Nav1.5 channels significantly decreased IK1, since they did not positively modulate Kir2.1/2.2 channels. Moreover, Golgi trafficking-defective Nav1.5 mutants produced a dominant negative effect on Kir2.1/2.2 and thus an additional IK1 reduction. Moreover, ER trafficking-defective Nav1.5 channels can be partially rescued by Kir2.1/2.2 channels through an unconventional secretory route that involves Golgi reassembly stacking proteins (GRASPs). Therefore, cardiac excitability would be greatly affected in subjects harboring Nav1.5 mutations with Golgi trafficking defects, since these mutants can concomitantly trap Kir2.1/2.2 channels, thus unexpectedly decreasing IK1 in addition to INa.

Published
2018

24. Human influenza A virus causes myocardial and cardiac-specific conduction system infections associated with early inflammation and premature death.

Author

Filgueiras-Rama, David, Vasilijevic, Jasmina, Jalife, Jose, Noujaim, Sami F, Alfonso, Jose M, Nicolas-Avila, Jose A, Gutierrez, Celia, Zamarreño, Noelia, Hidalgo, Andres, Bernabé, Alejandro, Cop, Christopher Pablo, Ponce-Balbuena, Daniela, Guerrero-Serna, Guadalupe, Calle, Daniel, Desco, Manuel, Ruiz-Cabello, Jesus, Nieto, Amelia, and Falcon, Ana

Subjects
EARLY death, INFLUENZA A virus, HEART conduction system, LYSYL oxidase, PURKINJE cells, RECOMBINANT viruses
Abstract

Aims Human influenza A virus (hIAV) infection is associated with important cardiovascular complications, although cardiac infection pathophysiology is poorly understood. We aimed to study the ability of hIAV of different pathogenicity to infect the mouse heart, and establish the relationship between the infective capacity and the associated in vivo , cellular and molecular alterations. Methods and results We evaluated lung and heart viral titres in mice infected with either one of several hIAV strains inoculated intranasally. 3D reconstructions of infected cardiac tissue were used to identify viral proteins inside mouse cardiomyocytes, Purkinje cells, and cardiac vessels. Viral replication was measured in mouse cultured cardiomyocytes. Human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) were used to confirm infection and study underlying molecular alterations associated with the in vivo electrophysiological phenotype. Pathogenic and attenuated hIAV strains infected and replicated in cardiomyocytes, Purkinje cells, and hiPSC-CMs. The infection was also present in cardiac endothelial cells. Remarkably, lung viral titres did not statistically correlate with viral titres in the mouse heart. The highly pathogenic human recombinant virus PAmut showed faster replication, higher level of inflammatory cytokines in cardiac tissue and higher viral titres in cardiac HL-1 mouse cells and hiPSC-CMs compared with PB2mut-attenuated virus. Correspondingly, cardiac conduction alterations were especially pronounced in PAmut-infected mice, associated with high mortality rates, compared with PB2mut-infected animals. Consistently, connexin43 and NaV1.5 expression decreased acutely in hiPSC-CMs infected with PAmut virus. YEM1L protease also decreased more rapidly and to lower levels in PAmut-infected hiPSC-CMs compared with PB2mut-infected cells, consistent with mitochondrial dysfunction. Human IAV infection did not increase myocardial fibrosis at 4-day post-infection, although PAmut-infected mice showed an early increase in mRNAs expression of lysyl oxidase. Conclusion Human IAV can infect the heart and cardiac-specific conduction system, which may contribute to cardiac complications and premature death. [ABSTRACT FROM AUTHOR]

Published
2021
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25. Brugada syndrome trafficking–defective Nav1.5 channels can trap cardiac Kir2.1/2.2 channels

Author

Pérez-Hernández, Marta, primary, Matamoros, Marcos, additional, Alfayate, Silvia, additional, Nieto-Marín, Paloma, additional, Utrilla, Raquel G., additional, Tinaquero, David, additional, de Andrés, Raquel, additional, Crespo, Teresa, additional, Ponce-Balbuena, Daniela, additional, Willis, B. Cicero, additional, Jiménez-Vazquez, Eric N., additional, Guerrero-Serna, Guadalupe, additional, da Rocha, Andre M., additional, Campbell, Katherine, additional, Herron, Todd J., additional, Díez-Guerra, F. Javier, additional, Tamargo, Juan, additional, Jalife, José, additional, Caballero, Ricardo, additional, and Delpón, Eva, additional

Published
2018
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27. Cardiac Kir2.1 and Na V 1.5 Channels Traffic Together to the Sarcolemma to Control Excitability

Author

Ponce-Balbuena, Daniela, primary, Guerrero-Serna, Guadalupe, additional, Valdivia, Carmen R., additional, Caballero, Ricardo, additional, Diez-Guerra, F. Javier, additional, Jiménez-Vázquez, Eric N., additional, Ramírez, Rafael J., additional, Monteiro da Rocha, André, additional, Herron, Todd J., additional, Campbell, Katherine F., additional, Willis, B. Cicero, additional, Alvarado, Francisco J., additional, Zarzoso, Manuel, additional, Kaur, Kuljeet, additional, Pérez-Hernández, Marta, additional, Matamoros, Marcos, additional, Valdivia, Héctor H., additional, Delpón, Eva, additional, and Jalife, José, additional

Published
2018
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29. Molecular and Electrophysiological Analyses of ATP2B4Gene Variants in Bilateral Adrenal Hyperaldosteronism

Author

Hattangady, Namita Ganesh, Foster, Jessica, Lerario, Antonio Marcondes, Ponce-Balbuena, Daniela, Rege, Juilee, Monticone, Silvia, Rainey, William E., Mulatero, Paolo, and Else, Tobias

Abstract

Primary aldosteronism (PA) is the most common cause of secondary hypertension with a high prevalence among patients with resistant hypertension. Despite the recent discovery of somatic variants in aldosterone-producing adenoma (APA)-associated PA, causes for PA due to bilateral aldosterone production (bilateral hyperaldosteronism; BHA) remain unknown. Herein, we identified rare gene variants in ATP2B4, in a cohort of patients with BHA. ATP2B4belongs to the same family of Ca-ATPases as ATP2B3, which is involved in the pathogenesis of APA. Endogenous ATP2B4expression was characterized in adrenal tissue, and the gene variants were functionally analyzed for effects on aldosterone synthase (CYP11B2) expression, steroid production in basal and agonist-stimulated conditions, and for changes in biophysical properties of channel properties. Knockdown of ATP2B4in HAC15 exhibited reduced angiotensin II stimulation in one of four shRNA clones. Stable HAC15 cell lines with doxycycline (dox) – inducible wild-type and variant forms of ATP2B4– were generated, and dox-induced upregulation of ATP2B4mRNA and protein was confirmed. However, ATP2B4variants did not alter basal or agonist-stimulated CYP11B2expression. Whole-cell recordings in HAC15 cells indicated robust endogenous ATP2B4conductance in native cells but reduced conductance with overexpressed WT and variant ATP2B4. The previously defined PA-causing ATP2B3variant served as a positive control and exhibited elevated CYP11B2mRNA. In conclusion, while this study did not confirm a pathogenic role for ATP2B4variants in BHA, we describe the sequencing analysis for familial and sporadic BHA and outline a template for the thorough in vitro characterization of gene variants.

Published
2020
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32. Constitutive Intracellular Na + Excess in Purkinje Cells Promotes Arrhythmogenesis at Lower Levels of Stress Than Ventricular Myocytes From Mice With Catecholaminergic Polymorphic Ventricular Tachycardia

Author

Willis, B. Cicero, primary, Pandit, Sandeep V., additional, Ponce-Balbuena, Daniela, additional, Zarzoso, Manuel, additional, Guerrero-Serna, Guadalupe, additional, Limbu, Bijay, additional, Deo, Makarand, additional, Camors, Emmanuel, additional, Ramirez, Rafael J., additional, Mironov, Sergey, additional, Herron, Todd J., additional, Valdivia, Héctor H., additional, and Jalife, José, additional

Published
2016
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33. Extracellular Matrix–Mediated Maturation of Human Pluripotent Stem Cell–Derived Cardiac Monolayer Structure and Electrophysiological Function

Author

Herron, Todd J., primary, Rocha, Andre Monteiro Da, additional, Campbell, Katherine F., additional, Ponce-Balbuena, Daniela, additional, Willis, B. Cicero, additional, Guerrero-Serna, Guadalupe, additional, Liu, Qinghua, additional, Klos, Matt, additional, Musa, Hassan, additional, Zarzoso, Manuel, additional, Bizy, Alexandra, additional, Furness, Jamie, additional, Anumonwo, Justus, additional, Mironov, Sergey, additional, and Jalife, José, additional

Published
2016
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34. Nav1.5 N-terminal domain binding to α1-syntrophin increases membrane density of human Kir2.1, Kir2.2 and Nav1.5 channels

Author

Matamoros, Marcos, primary, Pérez-Hernández, Marta, additional, Guerrero-Serna, Guadalupe, additional, Amorós, Irene, additional, Barana, Adriana, additional, Núñez, Mercedes, additional, Ponce-Balbuena, Daniela, additional, Sacristán, Sandra, additional, Gómez, Ricardo, additional, Tamargo, Juan, additional, Caballero, Ricardo, additional, Jalife, José, additional, and Delpón, Eva, additional

Published
2016
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35. Abstract 11513: Eplerenone Treatment Mitigates Atrial Structural Remodeling but Does Not Modify the Transition From Paroxysmal to Persistent Atrial Fibrillation in an Ovine Model

Author

Takemoto, Yoshio, primary, Ramirez, Rafael J, additional, Kaur, Kuljeet, additional, Ponce-Balbuena, Daniela, additional, Ramos-Mondragon, Roberto, additional, Willis, Byrd C, additional, Ennis, Steven R, additional, Guerrero-Serna, Guadalupe, additional, Pandit, Sandeep V, additional, Berenfeld, Omer, additional, and Jalife, José, additional

Published
2015
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37. Dominant Frequency Increase Rate Predicts Transition from Paroxysmal to Long-Term Persistent Atrial Fibrillation

Author

Martins, Raphael P., primary, Kaur, Kuljeet, additional, Hwang, Elliot, additional, Ramirez, Rafael J., additional, Willis, B. Cicero, additional, Filgueiras-Rama, David, additional, Ennis, Steven R., additional, Takemoto, Yoshio, additional, Ponce-Balbuena, Daniela, additional, Zarzoso, Manuel, additional, O’Connell, Ryan P., additional, Musa, Hassan, additional, Guerrero-Serna, Guadalupe, additional, Avula, Uma Mahesh R., additional, Swartz, Michael F., additional, Bhushal, Sandesh, additional, Deo, Makarand, additional, Pandit, Sandeep V., additional, Berenfeld, Omer, additional, and Jalife, José, additional

Published
2014
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39. Constitutive Intracellular Na+ Excess in Purkinje Cells Promotes Arrhythmogenesis at Lower Levels of Stress Than Ventricular Myocytes From Mice With Catecholaminergic Polymorphic Ventricular Tachycardia.

Author

Willis, B. Cicero, Pandit, Sandeep V., Ponce-Balbuena, Daniela, Zarzoso, Manuel, Guerrero-Serna, Guadalupe, Limbu, Bijay, Deo, Makarand, Camors, Emmanuel, Ramirez, Rafael J., Mironov, Sergey, Herron, Todd J., Valdivia, Héctor H., and Jalife, José

Published
2016
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40. Nav1.5 N-terminal domain binding to a1-syntrophin increasesmembrane density of human Kir2.1, Kir2.2 and Nav1.5 channels.

Author

Matamoros, Marcos, Pérez-Hernández, Marta, Guerrero-Serna, Guadalupe, Amorós, Irene, Barana, Adriana, Núñez, Mercedes, Ponce-Balbuena, Daniela, Sacristán, Sandra, GÓmez, Ricardo, Tamargo, Juan, Caballero, Ricardo, Jalife, José, and DelpÓn, Eva

Subjects
SYNTROPHINS, HEART ventricles, MACROMOLECULAR dynamics, POTASSIUM, HEART cells
Abstract

Aims Cardiac excitability and refractoriness are largely determined by the function and number of inward rectifier K+ channels (Kir2.1-2.3), which are differentially expressed in the atria and ventricles, and Nav1.5 channels. We have focused on how Nav1.5 and Kir2.x function within a macromolecular complex by elucidating the molecular determinants that govern Nav1.5/Kir2.x reciprocal modulation. Methods and results The results demonstrate that there is an unexpected 'internal' PDZ-like binding domain located at the N-terminus of the Nav1.5 channel that mediates its binding to a1-syntrophin. Nav1.5 N-terminal domain, by itself (the 132 aa peptide) (Nter), exerts a 'chaperone-like' effect that increases sodium (INa) and inward rectifier potassium (IK1) currents by enhancing the expression of Nav1.5, Kir2.1, and Kir2.2 channels as demonstrated in Chinese hamster ovary (CHO) cells and in rat cardiomyocytes. Site-directed mutagenesis analysis demonstrates that the Nter chaperone-like effect is determined by Serine 20. Nav1.5-Kir2.x reciprocal positive interactions depend on a specific C-terminal PDZ-binding domain sequence (SEI), which is present in Kir2.1 and Kir2.2 channels but not in Kir2.3. Therefore, in human atrial myocytes, the presence of Kir2.3 isoforms precludes reciprocal IK1-INa density modulation. Moreover, results in rat and human atrial myocytes demonstrate that binding to a1-syntrophin is necessary for the Nav1.5-Kir2.x-positive reciprocal modulation. Conclusions The results demonstrate the critical role of the N-terminal domain of Nav1.5 channels in Nav1.5-Kir2.x-reciprocal interactions and suggest that the molecular mechanisms controlling atrial and ventricular cellular excitability may be different. [ABSTRACT FROM AUTHOR]

Published
2016
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43. Specific residues of the cytoplasmic domains of cardiac inward rectifier potassium channels are effective antifibrillatory targets

Author

Noujaim, Sami F., primary, Stuckey, Jeanne A., additional, Ponce‐Balbuena, Daniela, additional, Ferrer‐Villada, Tania, additional, López‐Izquierdo, Angelica, additional, Pandit, Sandeep, additional, Calvo, Conrado J., additional, Grzeda, Krzysztof R., additional, Berenfeld, Omer, additional, Sánchez Chapula, José A., additional, and Jalife, José, additional

Published
2010
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46. Constitutive Intracellular Na+Excess in Purkinje Cells Promotes Arrhythmogenesis at Lower Levels of Stress Than Ventricular Myocytes From Mice With Catecholaminergic Polymorphic Ventricular Tachycardia

Author

Willis, B. Cicero, Pandit, Sandeep V., Ponce-Balbuena, Daniela, Zarzoso, Manuel, Guerrero-Serna, Guadalupe, Limbu, Bijay, Deo, Makarand, Camors, Emmanuel, Ramirez, Rafael J., Mironov, Sergey, Herron, Todd J., Valdivia, Héctor H., and Jalife, José

Abstract

Supplemental Digital Content is available in the text.

Published
2016
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47. Carvedilol inhibits Kir2.3 channels by interference with PIP2-channel interaction

Author

Ferrer, Tania, Ponce-Balbuena, Daniela, López-Izquierdo, Angélica, Aréchiga-Figueroa, Ivan A., de Boer, Teun P., van der Heyden, Marcel A.G., and Sánchez-Chapula, José A.

Subjects
*ADRENERGIC beta blockers, *ADRENERGIC receptors, *MEMBRANE proteins, *PROTEIN-protein interactions, *CONGESTIVE heart failure treatment, *HYPERTENSION, *MYOCARDIAL infarction, *GENETIC mutation
Abstract

Abstract: Carvedilol, a β- and α-adrenoceptor blocker, is used to treat congestive heart failure, mild to moderate hypertension, and myocardial infarction. It has been proposed to block KATP channels by binding to the bundle crossing region at a domain including cysteine at position 166, and thereby plugging the pore region. However, carvedilol was reported not to affect Kir2.1 channels, which lack 166 Cys. Here, we demonstrate that carvedilol inhibits Kir2.3 carried current by an alternative mechanism. Carvedilol inhibited Kir2.3 channels with at least 100 fold higher potency (IC50 =0.49μM) compared to that for Kir2.1 (IC50 >50μM). Kir2.3 channel inhibition was concentration-dependent and voltage-independent. Increasing Kir2.3 channel affinity for PIP2, by a I213L point mutation, decreased the inhibitory effect of carvedilol more than twentyfold (IC50 =11.1μM). In the presence of exogenous PIP2, Kir2.3 channel inhibition by carvedilol was strongly reduced (80 vs. 2% current inhibition). These results suggest that carvedilol, as other cationic amphiphilic drugs, inhibits Kir2.3 channels by interfering with the PIP2-channel interaction. [Copyright &y& Elsevier]

Published
2011
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49. The Antimalarial Drug Mefloquine Inhibits Cardiac Inward Rectifier K+Channels Evidence for Interference in PIP2-Channel Interaction

Author

López-Izquierdo, Angélica, Ponce-Balbuena, Daniela, Moreno-Galindo, Eloy G, Aréchiga-Figueroa, Iván A, Rodríguez-Martínez, Martín, Ferrer, Tania, Rodríguez-Menchaca, Aldo A, and Sánchez-Chapula, José A

Abstract

The antimalarial drug mefloquine was found to inhibit the KATPchannel by an unknown mechanism. Because mefloquine is a Cationic amphiphilic drug and is known to insert into lipid bilayers, we postulate that mefloquine interferes with the interaction between PIP2and Kir channels resulting in channel inhibition. We studied the inhibitory effects of mefloquine on Kir2.1, Kir2.3, Kir2.3(I213L), and Kir6.2/SUR2A channels expressed in HEK-293 cells, and on IK1and IKATPfrom feline cardiac myocytes. The order of mefloquine inhibition was Kir6.2/SUR2A Kir2.3 (IC502 μM) > Kir2.1 (IC50> 30 μM). Similar results were obtained in cardiac myocytes. The Kir2.3(I213L) mutant, which enhances the strength of interaction with PIP2(compared to WT), was significantly less sensitive (IC50= 9 μM). In inside-out patches, continuous application of PIP2strikingly prevented the mefloquine inhibition. Our results support the idea that mefloquine interferes with PIP2-Kir channels interactions.

Published
2011
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50. Tamoxifen Inhibits Cardiac ATP-Sensitive and Acetylcholine-Activated K+Currents in Part by Interfering With Phosphatidylinositol 4,5-Bisphosphate–Channel Interaction

Author

Ponce-Balbuena, Daniela, Moreno-Galindo, Eloy G., López-Izquierdo, Angélica, Ferrer, Tania, and Sánchez-Chapula, José A.

Abstract

Tamoxifen inhibits transmembrane currents of the Kir2.x inward rectifier potassium channels by interfering with the interaction of the channels with membrane phosphatidylinositol 4,5-bisphosphate (PIP2). We tested the hypothesis that Kir channels with low affinity for PIP2, like the adenosine triphosphate (ATP)-sensitive K+channel (KATP) and acetylcholine (ACh)-activated K+channel (KACh), have at least the same sensitivity to tamoxifen as Kir2.3. We investigated the effects of tamoxifen (0.1 – 10 μM) on Kir6.2/SUR2A (KATP) and Kir3.1/3.4 (KACh) channels expressed in HEK-293 cells and ATP-sensitive K+current (IKATP) and ACh-activated K+current (IKACh) in feline atrial myocytes. The onset of tamoxifen inhibition of both IKATPand IKAChwas slow (T1/2approximately 3.5 min) and concentration-dependent but voltage-independent. The time course and degree of inhibition was independent of external or internal drug application. Tamoxifen interacts with the pore forming subunit, Kir6.2, rather than with the SUR subunit. The inhibitory potency of tamoxifen on the Kir6.2/SUR2A channel was decreased by the mutation (C166S) on Kir6.2 and in the continuous presence of PIP2. In atrial myocytes, the mechanism and potency of the effects of tamoxifen on KATPand KAChchannels were comparable to those in HEK-293 cells. These data suggest that, similar to its effects on Kir2.x currents, tamoxifen inhibits KATPand KAChcurrents by interfering with the interaction between the channel and PIP2.

Published
2010
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