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1. Stromal Cell-SLIT3/Cardiomyocyte-ROBO1 Axis Regulates Pressure Overload-Induced Cardiac Hypertrophy

Author

Liu, Xiaoxiao, Li, Baolei, Wang, Shuyun, Zhang, Erge, Schultz, Megan, Touma, Marlin, Da Rocha, Andre Monteiro, Evans, Sylvia M, Eichmann, Anne, Herron, Todd, Chen, Ruizhen, Xiong, Dingding, Jaworski, Alexander, Weiss, Stephen, and Si, Ming-Sing

Subjects
Biomedical and Clinical Sciences, Medical Physiology, Cardiovascular Medicine and Haematology, Genetics, Pediatric, Cardiovascular, Heart Disease, Heart Disease - Coronary Heart Disease, Aetiology, 2.1 Biological and endogenous factors, Animals, Humans, Mice, Cardiomegaly, Cells, Cultured, Disease Models, Animal, Fibrosis, Hypertrophy, Left Ventricular, Membrane Proteins, Mice, Inbred C57BL, Mice, Knockout, Myocytes, Cardiac, Nerve Tissue Proteins, Receptors, Immunologic, Ventricular Remodeling, ROBO1, axon guidance, fibroblasts, fibrosis, myocytes, cardiac, stromal cells, ventricular pressure, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Clinical sciences
Abstract

BackgroundRecently shown to regulate cardiac development, the secreted axon guidance molecule SLIT3 maintains its expression in the postnatal heart. Despite its known expression in the cardiovascular system after birth, SLIT3's relevance to cardiovascular function in the postnatal state remains unknown. As such, the objectives of this study were to determine the postnatal myocardial sources of SLIT3 and to evaluate its functional role in regulating the cardiac response to pressure overload stress.MethodsWe performed in vitro studies on cardiomyocytes and myocardial tissue samples from patients and performed in vivo investigation with SLIT3 and ROBO1 (roundabout homolog 1) mutant mice undergoing transverse aortic constriction to establish the role of SLIT3-ROBO1 in adverse cardiac remodeling.ResultsWe first found that SLIT3 transcription was increased in myocardial tissue obtained from patients with congenital heart defects that caused ventricular pressure overload. Immunostaining of hearts from WT (wild-type) and reporter mice revealed that SLIT3 is secreted by cardiac stromal cells, namely fibroblasts and vascular mural cells, within the heart. Conditioned media from cardiac fibroblasts and vascular mural cells both stimulated cardiomyocyte hypertrophy in vitro, an effect that was partially inhibited by an anti-SLIT3 antibody. Also, the N-terminal, but not the C-terminal, fragment of SLIT3 and the forced overexpression of SLIT3 stimulated cardiomyocyte hypertrophy and the transcription of hypertrophy-related genes. We next determined that ROBO1 was the most highly expressed roundabout receptor in cardiomyocytes and that ROBO1 mediated SLIT3's hypertrophic effects in vitro. In vivo, Tcf21+ fibroblast and Tbx18+ vascular mural cell-specific knockout of SLIT3 in mice resulted in decreased left ventricular hypertrophy and cardiac fibrosis after transverse aortic constriction. Furthermore, α-MHC+ cardiomyocyte-specific deletion of ROBO1 also preserved left ventricular function and abrogated hypertrophy, but not fibrosis, after transverse aortic constriction.ConclusionsCollectively, these results indicate a novel role for the SLIT3-ROBO1-signaling axis in regulating postnatal cardiomyocyte hypertrophy induced by pressure overload.

Published
2024

4. Repolarization studies using human stem cell-derived cardiomyocytes: Validation studies and best practice recommendations

Author

Gintant, Gary, Kaushik, Emily Pfeiffer, Feaster, Tromondae, Stoelzle-Feix, Sonja, Kanda, Yasunari, Osada, Tomoharu, Smith, Godfrey, Czysz, Katherine, Kettenhofen, Ralf, Lu, Hua Rong, Cai, Beibei, Shi, Hong, Herron, Todd Joseph, Dang, Qianyu, Burton, Francis, Pang, Li, Traebert, Martin, Abassi, Yama, Pierson, Jennifer Beck, and Blinova, Ksenia

Published
2020
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8. 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

10. Biobank-driven genomic discovery yields new insight into atrial fibrillation biology

Author

Nielsen, Jonas B., Thorolfsdottir, Rosa B., Fritsche, Lars G., Zhou, Wei, Skov, Morten W., Graham, Sarah E., Herron, Todd J., McCarthy, Shane, Schmidt, Ellen M., Sveinbjornsson, Gardar, Surakka, Ida, Mathis, Michael R., Yamazaki, Masatoshi, Crawford, Ryan D., Gabrielsen, Maiken E., Skogholt, Anne Heidi, Holmen, Oddgeir L., Lin, Maoxuan, Wolford, Brooke N., Dey, Rounak, Dalen, Håvard, Sulem, Patrick, Chung, Jonathan H., Backman, Joshua D., Arnar, David O., Thorsteinsdottir, Unnur, Baras, Aris, O’Dushlaine, Colm, Holst, Anders G., Wen, Xiaoquan, Hornsby, Whitney, Dewey, Frederick E., Boehnke, Michael, Kheterpal, Sachin, Mukherjee, Bhramar, Lee, Seunggeun, Kang, Hyun M., Holm, Hilma, Kitzman, Jacob, Shavit, Jordan A., Jalife, José, Brummett, Chad M., Teslovich, Tanya M., Carey, David J., Gudbjartsson, Daniel F., Stefansson, Kari, Abecasis, Gonçalo R., Hveem, Kristian, and Willer, Cristen J.

Published
2018
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14. Contributors

Author

Aagaard, Philip, primary, Abrams, Dominic James, additional, Abriel, Hugues, additional, Adkisson, Wayne O., additional, Agullo-Pascual, Esperanza, additional, Alvarado, Francisco J., additional, Amin, Ahmad S., additional, Antzelevitch, Charles, additional, Anumonwo, Justus M.B., additional, Armaganijan, Luciana, additional, Arya, Arash, additional, Asirvatham, Samuel, additional, Atienza, Felipe, additional, Backx, Peter H., additional, Ballou, Lisa M., additional, Balse, Elise, additional, Balulad, Sujata, additional, Barbuti, Andrea, additional, Bardy, Gust H., additional, Bassil, Guillaume, additional, Benditt, David G., additional, Berenfeld, Omer, additional, Bers, Donald M., additional, Binah, Ofer, additional, Bogun, Frank, additional, Bongianino, Rossana, additional, Boyle, Noel G., additional, Boyle, Patrick M., additional, Breithardt, Günter, additional, Brini, Marisa, additional, Brink, Peter R., additional, Brugada, Pedro, additional, Buch, Eric, additional, Bukauskas, Feliksas F., additional, Calkins, Hugh, additional, Callans, David J., additional, Caples, Sean M., additional, Carafoli, Ernesto, additional, Catterall, William A., additional, Cerrone, Marina, additional, Chaumeil, Arnaud, additional, Chen, Caressa, additional, Chen, Lan S., additional, Chen, Peng-Sheng, additional, Cheng, Jianding, additional, Chiamvimonvat, Nipavan, additional, Christini, David J., additional, Chugh, Aman, additional, Climent, Andreu M., additional, Cohen, Ira S., additional, Connolly, Stuart J., additional, Cooper, Lebron, additional, Crespo, Eric M., additional, Crotti, Lia, additional, Csepe, Thomas A., additional, Cuoco, Frank, additional, Curtis, Anne B., additional, Damiano, Ralph J., additional, Darbar, Dawood, additional, Das, Mithilesh K., additional, d’Avila, Andre, additional, Delmar, Mario, additional, Delpón, Eva, additional, Denegri, Marco, additional, Denis, Arnaud, additional, Derval, Nicolas, additional, Deschênes, Isabelle, additional, Deshmukh, Abhishek, additional, Di Biase, Luigi, additional, Dickfeld, Timm M., additional, Dierckx, Hans, additional, Dinov, Borislav, additional, Dixit, Sanjay, additional, Dobrev, Dobromir, additional, Dubois, Remi, additional, Eckardt, Lars, additional, Edwards, Andrew G., additional, Ellenbogen, Kenneth A., additional, Ellinor, Patrick T., additional, Estes, N.A. Mark, additional, Fabritz, Larissa, additional, Fedorov, Vadim V., additional, Fernandez, Antonio B., additional, Teijeira Fernández, Elvis, additional, Filgueiras-Rama, David, additional, Fishbein, Michael C., additional, Fishman, Glenn I., additional, Frankel, David S., additional, Friedman, Paul, additional, Frontera, Antonio, additional, Gami, Apoor S., additional, Garabelli, Paul, additional, George, Alfred L., additional, Gerstenfeld, Edward P., additional, Gizurarson, Sigfus, additional, Gold, Michael R., additional, Goldberger, Jeffrey J., additional, Grace, Andrew, additional, Grassi, Guido, additional, Greenfield, Ruth Ann, additional, Gross, Wendy L., additional, Grubb, Blair P., additional, Guillem, María S., additional, Györke, Sándor, additional, Haïssaguerre, Michel, additional, Hake, Johan, additional, Halperin, Henry R., additional, Hansen, Brian J., additional, Hatem, Stéphane, additional, Hayes, David L., additional, Heijman, Jordi, additional, Herron, Todd J., additional, Hindricks, Gerhard, additional, Hocini, Mélèze, additional, Hohnloser, Stefan H., additional, Holmes, David R., additional, Hoshijima, Masahiko, additional, Hund, Thomas J., additional, Hutchinson, Mathew D., additional, Ilkhanoff, Leonard, additional, Ingles, Jodie, additional, Ip, James E., additional, Jackman, Warren M., additional, Jackson, Nicholas, additional, Jaïs, Pierre, additional, Jalife, José, additional, Jhun, Bong Sook, additional, John, Roy M., additional, Jongbloed, Monique, additional, Jordaens, Luc, additional, Kalman, Jonathan M., additional, Kamp, Timothy J., additional, Kanj, Mohamed H., additional, Kapa, Suraj, additional, Karabin, Beverly, additional, Karakikes, Ioannis, additional, Katritsis, Demosthenes G., additional, Kaur, Kuljeet, additional, Kirchhof, Paulus, additional, Kléber, André G., additional, Klein, George J., additional, Kohl, Peter, additional, Koneru, Jayanthi N., additional, Koruth, Jacob S., additional, Krahn, Andrew D., additional, Krogh-Madsen, Trine, additional, Kuck, Karl Heinz, additional, Kumar, Saurabh, additional, Kushnir, Alexander, additional, Lakdawala, Neal K., additional, Laksman, Zachary W.M., additional, Latchamsetty, Rakesh, additional, Lau, Dennis H., additional, Lerman, Bruce B., additional, Lin, Richard Z., additional, Lin, Shien-Fong, additional, Link, Mark S., additional, Liu, Bin, additional, Liu, Christopher F., additional, Lockwood, Deborah J., additional, Lopatin, Anatoli N., additional, Lubitz, Steven A., additional, Mahajan, Rajiv, additional, Makielski, Jonathan C., additional, Malik, Marek, additional, Marchlinski, Francis E., additional, Markowitz, Steven M., additional, Maron, Barry J., additional, Maron, Martin S., additional, Marx, Steven O., additional, Massé, Stéphane, additional, McCulloch, Andrew D., additional, McKelvie-Sebileau, Pippa, additional, Melby, Spencer J., additional, Metzner, Andreas, additional, Michailova, Anushka P., additional, Michaud, Gregory F., additional, Miller, John M., additional, Mishra, Jyotsna, additional, Mitrani, Raul D., additional, Mohler, Peter J., additional, Morady, Fred, additional, Myerburg, Robert J., additional, Nakagawa, Hiroshi, additional, Nalliah, Chrishan Joseph, additional, Nanthakumar, Kumaraswamy, additional, Napolitano, Carlo, additional, Narayan, Sanjiv M., additional, Natale, Andrea, additional, Nattel, Stanley, additional, Nazarian, Saman, additional, Nguyen, Thao P., additional, Nogami, Akihiko, additional, Noujaim, Sami F., additional, Nubret Le Coniat, Karine, additional, Olshansky, Brian, additional, O-Uchi, Jin, additional, Oudit, Gavin Y., additional, Ouyang, Feifan, additional, Ozcan, Cevher, additional, Packer, Douglas L., additional, Pandit, Sandeep V., additional, Panfilov, Alexander V., additional, Park, David S., additional, Patocskai, Bence, additional, Pauza, Dainius H., additional, Pauziene, Neringa, additional, Piccini, Jonathan P., additional, Pitt, Geoffrey S., additional, Po, Sunny S., additional, Prasad, Abhiram, additional, Priori, Silvia G., additional, Radwański, Przemysław B., additional, Rappel, Wouter-Jan, additional, Reiser, Michelle, additional, Restrepo, Alejandro Jimenez, additional, Robinson, Richard B., additional, Roden, Dan M., additional, Rosen, Michael R., additional, Rosso, Raphael, additional, Rudy, Yoram, additional, Rysevaite-Kyguoliene, Kristina, additional, Sabbah, Hani N., additional, Sacher, Frederic, additional, Sachse, Frank B., additional, Saguner, Ardan M., additional, Sanders, Prashanthan, additional, Sanguinetti, Michael C., additional, Santangeli, Pasquale, additional, Sarraf, Mohammad, additional, Satin, Jonathan, additional, Schalij, Martin Jan, additional, Scherlag, Benjamin J., additional, Schill, Matthew R., additional, Schleifer, J. William, additional, Schuessler, Richard B., additional, Schwartz, Peter J., additional, Seeger, Timon, additional, Semsarian, Christopher, additional, Seravalle, Gino, additional, Shah, Ashok J., additional, Shaw, Robin M., additional, Shen, Mark J., additional, Shen, Win–Kuang, additional, Sheu, Shey-Shing, additional, Shivkumar, Kalyanam, additional, Silva, Jennifer N.A., additional, Skanes, Allan C., additional, Soejima, Kyoko, additional, Somers, Virend K., additional, Sorajja, Dan, additional, Stavrakis, Stavros, additional, Steinberg, Christian, additional, Stevenson, Lynne Warner, additional, Stevenson, William G., additional, Sweeney, Michael O., additional, Swerdlow, Charles, additional, Takigawa, Masateru, additional, Tamargo, Juan, additional, Tandri, Harikrishna, additional, Tedrow, Usha B., additional, Thompson, Nathaniel, additional, Thompson, Paul D., additional, Tomaselli, Gordon F., additional, Towbin, Jeffrey A., additional, Trayanova, Natalia A., additional, Tristani-Firouzi, Martin, additional, Tseng, Zian H., additional, Ueda, Akiko, additional, Valdivia, Héctor H., additional, Valiunas, Virginijus, additional, van der Werf, Christian, additional, Van Hare, George F., additional, Vidmar, David, additional, Viskin, Sami, additional, Voigt, Niels, additional, Walsh, Edward P., additional, Wang, Paul J., additional, Wehrens, Xander H.T., additional, Weiss, Mark S., additional, Wilde, Arthur A.M., additional, Wilkoff, Bruce L., additional, Woo, Y. Joseph, additional, Wu, Joseph C., additional, Yee, Raymond, additional, Zaman, Junaid A.B., additional, Zarzoso, Manuel, additional, Zeitler, Emily P., additional, Zeppenfeld, Katja, additional, Zghaib, Tarek, additional, Zhang, Xiao-Dong, additional, and Zipes, Douglas P., additional

Published
2018
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17. Mitochondrial oxidative stress contributes to diastolic dysfunction through impaired mitochondrial dynamics

Author

Lozhkin, Andrey, primary, Vendrov, Aleksandr E., additional, Ramos-Mondragón, R., additional, Canugovi, Chandrika, additional, Stevenson, Mark D., additional, Herron, Todd J., additional, Hummel, Scott L., additional, Figueroa, C Alberto, additional, Bowles, Dawn E., additional, Isom, Lori L., additional, Runge, Marschall S., additional, and Madamanchi, Nageswara R., additional

Published
2022
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18. 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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20. 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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24. 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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26. 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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28. Loss of H3K4 methylation destabilizes gene expression patterns and physiological functions in adult murine cardiomyocytes

Author

Stein, Adam B., Jones, Thomas A., Herron, Todd J., Patel, Sanjeevkumar R., Day, Sharlene M., Noujaim, Sami F., Milstein, Michelle L., Klos, Matthew, Furspan, Philip B., Jalife, Jose, and Dressler, Gregory R.

Subjects
Gene expression -- Physiological aspects -- Research, Methylation -- Research, Histones -- Physiological aspects -- Research, Heart cells -- Physiological aspects -- Genetic aspects -- Research, Methyltransferases -- Physiological aspects -- Research, Health care industry
Abstract

Histone H3 lysine 4 (H3K4me) methyltransferases and their cofactors are essential for embryonic development and the establishment of gene expression patterns in a cell-specific and heritable manner. However, the importance [...]

Published
2011
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29. 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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31. Power output is linearly related to MyHC content in rat skinned myocytes and isolated working hearts

Author

Korte, F. Steven, Herron, Todd J., Rovetto, Michael J., and McDonald, Kerry S.

Subjects
Myosin, Heart muscle, Muscle proteins, Biological sciences
Abstract

The amount of work the heart can perform during ejection is governed by the inherent contractile properties of individual myocytes. One way to alter contractile properties is to alter contractile proteins such as myosin heavy chain (MyHC), which is known to demonstrate isoform plasticity in response to disease states. The purpose of this study was to examine myocyte functionality over the complete range of MyHC expression in heart, from 100% [alpha]-MyHC to 100% [beta]-MyHC, using euthyroid and hypothyroid rats. Peak power output in skinned cardiac myocytes decreased as a nearly linear function of [beta]-MyHC expression during maximal ([r.sup.2] = 0.85, n = 44 myocyte preparations) and submaximal ([r.sup.2] = 0.82, n = 31 myocyte preparations) [Ca.sup.2+] activation. To determine whether single myocyte function translated to the level of the whole heart, power output was measured in working heart preparations expressing varied ratios of MyHC. Left ventricular power output of isolated working heart preparations also decreased as a linear function of increasing [beta]-MyHC expression ([r.sup.2] = 0.82, n = 34 myocyte preparations). These results demonstrate that power output is highly dependent on MyHC expression in single myocytes, and this translates to the performance of working left ventricles. myosin heavy chain; myocardium; myocardial contractility; cardiac muscle

Published
2005

33. Abnormal myocardial expression of SAP97 is associated with arrhythmogenic risk

Author

Musa, Hassan, primary, Marcou, Cherisse A., additional, Herron, Todd J., additional, Makara, Michael A., additional, Tester, David J., additional, O’Connell, Ryan P., additional, Rosinski, Brad, additional, Guerrero-Serna, Guadalupe, additional, Milstein, Michelle L, additional, Monteiro da Rocha, André, additional, Ye, Dan, additional, Crotti, Lia, additional, Nesterenko, Vladislav V., additional, Castelletti, Silvia, additional, Torchio, Margherita, additional, Kotta, Maria-Christina, additional, Dagradi, Federica, additional, Antzelevitch, Charles, additional, Mohler, Peter J., additional, Schwartz, Peter J., additional, Ackerman, Michael J., additional, and Anumonwo, Justus M., additional

Published
2020
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38. Contributors

Author

Abrams, Dominic, Abriel, Hugues, Adkisson, Wayne O., Ajijola, Olujimi A., Alvarado, Francisco J., Amin, Ahmad S., André, Clémentine, Anter, Elad, Antzelevitch, Charles, Ariga, Rina, Arora, Rishi, Arya, Arash, Asirvatham, Samuel, Atienza, Felipe, Atluri, Pavan, Balse, Elise, Basso, Cristina, Benditt, David G., Bennett, Richard, Berenfeld, Omer, Berruezo, Antonio, Bers, Donald M., Bhaskaran, Ashwin, Bogun, Frank, Bose, Rupan, Botzer, Lior, Boyle, Patrick M., Bradfield, Jason S., Brini, Marisa, Brugada, Pedro, Caldwell, Jessica L., Calkins, Hugh, Poindexter, Catherine Ellen, Callans, David J., Carafoli, Ernesto, Catterall, William A., Cerrone, Marina, Chandler, Stephanie, Chauvel, Remi, Chen, Lan S., Chen, Peng-Sheng, Cheniti, Ghassen, Cheung, Christopher C., Chiamvimonvat, Nipavan, Chiang, David Y., Chorin, Ehud, Christini, David J., Christoffels, Vincent M., Christoph, Jan, Clancy, Colleen E., Climent, Andreu M., Cochet, Hubert, Coetzee, William A., Crossley, George H., Crotti, Lia, Cuculich, Phillip S., Curtis, Anne B., Dagradi, Federica, Damiano, Ralph J., Jr, Darbar, Dawood, Das, Mithilesh K., Delmar, Mario, Delpón, Eva, Derval, Nicolas, Deshmukh, Abhishek, Dherange, Parinita, Dickfeld, Timm M., Dierckx, Hans, Dinov, Borislav, Divakaran, Sanjay, Dixit, Sanjay, Dubois, Rémi, Duchateau, Josselin, Edwards, Andrew G., Ellenbogen, Kenneth A., Ellinor, Patrick T., Ellis, Christopher R., Enriquez, Andres, Estes III, N.A. Mark, Etheridge, Susan P., Everett, Thomas H., Fedorov, Vadim V., Filgueiras-Rama, David, Fishbein, Michael, Fishman, Glenn I., Fradley, Michael, Gami, Apoor S., Gando, Ivan, Garabelli, Paul James, Garcia, Fermin, George, Alfred L., Jr, Gerstenfeld, Edward P., Goldberger, Jeffrey J., Gourdie, Robert G., Grace, Andrew, Grubb, Blair P., Guerrier, Karine, Guillem, María S., Györke, Sándor, Haines, David E., Halperin, Henry R., Hatem, Stéphane, Haïssaguerre, Michel, Herron, Todd J., Hindricks, Gerhard, Hocini, Mélèze, Hoffman, Jacob, Hund, Thomas J., Hutchinson, Mathew D., Iliceto, Sabino, Ilkhanoff, Leonard, Ingles, Jodie, Ip, James E., Jackman, Warren M., Jalife, Jose, Jaïs, Pierre, Jhun, Bong Sook, Restrepo, Alejandro Jimenez, John, Roy M., Johnson, Jason, Jongbloed, Monique, Jáuregui, Beatriz, Kalman, Jonathan M., Kalyanasundaram, Anuradha, Kamp, Timothy J., Kanagasundram, Arvindh N., Kang, Po Wei, Kanj, Mohamed H., Kapa, Suraj, Kapur, Sunil, Karabin, Beverly, Kernik, Divya C., Klein, George J., Kléber, André G., Knight, Bradley P., Koenig, Sara N., Kohl, Peter, Konecny, Thomas, Koneru, Jayanthi N., Krahn, Andrew D., Krishnappa, Darshan, Krogh-Madsen, Trine, Kumar, Saurabh, Kusayama, Takashi, Kushnir, Alexander, Kwak, Brenda R., Lador, Adi, Lakatta, Edward G., Laksman, Zachary W.M., Latchamsetty, Rakesh, Lau, Dennis H., Lee, Byron K., Lenaeus, Michael J., Lerman, Bruce B., Li, Ning, Lin, Shien-Fong, Link, Mark S., Liu, Bin, Liu, Christopher F., Lockwood, Deborah J., Loeys, Bart, Lubitz, Steven A., Prof-Dr, Stefan Luther, Lyon, Aurore, MacGregor, Robert M., MacRae, Calum A., Maher, Timothy, Maltsev, Victor, Man, Joyce C.K., Marchlinski, Francis E., Markowitz, Steven M., Maron, Barry J., Maron, Martin S., Marra, Martina Perazzolo, Marx, Steven O., Mazzanti, Andrea, McCulloch, Andrew D., Mehta, Nishaki K., Melby, Spencer J., Mellor, Greg, Michaud, Gregory F., Miles, William M., Miller, Jennifer C., Miller, John M., Mitrani, Raul D., Mohler, Peter J., Montgomery, Jay A., Moreno, Jonathan D., Murray, Katherine T., Myerburg, Robert J., Nakagawa, Hiroshi, Naksuk, Niyada, Nalliah, Chrishan Joseph, Napolitano, Carlo, Narayan, Sanjiv M., Nazarian, Saman, Nerbonne, Jeanne M., Nery, Pablo B., Nguyen, Thao P., Nichols, Colin G., Nielsen, Morten S., Nogami, Akihiko, Noujaim, Sami F., Nubret, Karine, O-Uchi, Jin, Olgin, Jeffrey E., Olshansky, Brian, Ozcan, Cevher, Pambrun, Thomas, Panfilov, Alexander V., Pang, Paul D., Park, David S., Parlitz, Ulrich, Patocskai, Bence, Pauziene, Neringa, Pauža, Dainius H., Penela, Diego, Peyronnet, Rémi, Pfenniger, Anna, Phillips, S. Tyler, Picard, François, Ploux, Sylvain, Po, Sunny S., Poelzing, Steven, Polina, Iuliia, Porta-Sánchez, Andreu, Prasad, Abhiram, Priori, Silvia G., Pérez-Hernández, Marta, Qian, Pierre C., Quintanilla, MScEng, Jorge G., Radwański, Przemysław B., Ramirez, F. Daniel, Rappel, Wouter-Jan, Richardson, Travis D., Ripplinger, Crystal M., Robinson, Clifford G., Roden, Dan M., Rodrigo, Miguel, Rodriguez, Blanca, Rosso, Raphael, Rowin, Ethan J., Rudy, Yoram, Rysevaite-Kyguoliene, Kristina, Sacher, Frédéric, Sadek, Mouhannad M., Sanders, Prashanthan, Satin, Jonathan, Sauer, William H., Saxon, Leslie A., Schalij, Martin Jan, Schepers, Dorien, Scherlag, Benjamin J., Schleifer, J. William, Schmidt, Ehud J., Schröder-Schetelig, Johannes, Schuessler, Richard B., Schwartz, Peter J., Semsarian, Christopher, Shaw, Robin M., Shen, Win-Kuang, Sheu, Shey-Shing, Shivkumar, Kalyanam, Sieliwonczyk, Ewa, Silva, Jonathan R., Skanes, Allan C., Smyth, James W., Sobie, Eric A., Soejima, Kyoko, Somers, Virend K., Sorajja, Dan, Sroubek, Jakub, Stavrakis, Stavros, Steinberg, Christian, Stevenson, William G., Supple, Gregory E., Swerdlow, Charles, Tandri, Harikrishna, Tedrow, Usha, Thai, Phung N., Thiene, Gaetano, Tixier, Romain, Tomaselli, Gordon F., Towbin, Jeffrey A., Trayanova, Natalia A., Tristani-Firouzi, Martin, Tseng, Zian H., Tung, Roderick, Ueda, Akiko, Upadhyay, Gaurav A., Valderrábano, Miguel, Valdivia, Héctor H., van den Brink, Jonas, van der Werf, Christian, van Opbergen, Chantal J.M., Vaseghi, Marmar, Vautier, R. Ashton, Vera Pedrosa, Maria Linarejos, Verma, Nishant, Vermij, Sarah H., Virk, Sohaib, Viskin, Sami, Vlachos, Konstantinos, Walsh, Edward P., Wang, Paul J., Welte, Nicolas, Wilde, Arthur A.M., Wilkoff, Bruce L., Wu, Joseph C., Yang, Hua-Qian, Yee, Raymond, Zaman, Junaid A.B., Zeppenfeld, Katja, Zghaib, Tarek, Zhang, Jianhua, Zhang, Xiao-Dong, and Zimetbaum, Peter

Published
2022
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39. 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

41. HDAC inhibitor valproic acid protects heart function through Foxm1 pathway after acute myocardial infarction

Author

Tian, Shuo, primary, Lei, Ienglam, additional, Gao, Wenbin, additional, Liu, Liu, additional, Guo, Yijing, additional, Creech, Jeffery, additional, Herron, Todd J., additional, Xian, Shaoxiang, additional, Ma, Peter X., additional, Eugene Chen, Y., additional, Li, Yongqing, additional, Alam, Hasan B., additional, and Wang, Zhong, additional

Published
2019
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42. Genome-wide Study of Atrial Fibrillation Identifies Seven Risk Loci and Highlights Biological Pathways and Regulatory Elements Involved in Cardiac Development

Author

Nielsen, Jonas B., Fritsche, Lars G., Zhou, Wei, Teslovich, Tanya M., Holmen, Oddgeir L., Gustafsson, Stefan, Gabrielsen, Maiken E., Schmidt, Ellen M., Beaumont, Robin, Wolford, Brooke N., Lin, Maoxuan, Brummett, Chad M., Preuss, Michael H., Refsgaard, Lena, Bottinger, Erwin P., Graham, Sarah E., Surakka, Ida, Chu, Yunhan, Skogholt, Anne Heidi, Dalen, Havard, Boyle, Alan P., Oral, Hakan, Herron, Todd J., Kitzman, Jacob, Jalife, Jose, Svendsen, Jesper H., Olesen, Morten S., Njolstad, Inger, Lochen, Maja-Lisa, Baras, Aris, Gottesman, Omri, Marcketta, Anthony, O'Dushlaine, Colm, Ritchie, Marylyn D., Wilsgaard, Tom, Loos, Ruth J. F., Frayling, Timothy M., Boehnke, Michael, Ingelsson, Erik, Carey, David J., Dewey, Frederick E., Kang, Hyun M., Abecasis, Goncalo R., Hveem, Kristian, Willer, Cristen J., Nielsen, Jonas B., Fritsche, Lars G., Zhou, Wei, Teslovich, Tanya M., Holmen, Oddgeir L., Gustafsson, Stefan, Gabrielsen, Maiken E., Schmidt, Ellen M., Beaumont, Robin, Wolford, Brooke N., Lin, Maoxuan, Brummett, Chad M., Preuss, Michael H., Refsgaard, Lena, Bottinger, Erwin P., Graham, Sarah E., Surakka, Ida, Chu, Yunhan, Skogholt, Anne Heidi, Dalen, Havard, Boyle, Alan P., Oral, Hakan, Herron, Todd J., Kitzman, Jacob, Jalife, Jose, Svendsen, Jesper H., Olesen, Morten S., Njolstad, Inger, Lochen, Maja-Lisa, Baras, Aris, Gottesman, Omri, Marcketta, Anthony, O'Dushlaine, Colm, Ritchie, Marylyn D., Wilsgaard, Tom, Loos, Ruth J. F., Frayling, Timothy M., Boehnke, Michael, Ingelsson, Erik, Carey, David J., Dewey, Frederick E., Kang, Hyun M., Abecasis, Goncalo R., Hveem, Kristian, and Willer, Cristen J.

Abstract

Atrial fibrillation (AF) is a common cardiac arrhythmia and a major risk factor for stroke, heart failure, and premature death. The pathogenesis of AF remains poorly understood, which contributes to the current lack of highly effective treatments. To understand the genetic variation and biology underlying AF, we undertook a genome-wide association study (GWAS) of 6,337 AF individuals and 61,607 AF-free individuals from Norway, including replication in an additional 30,679 AF individuals and 278,895 AF-free individuals. Through genotyping and dense imputation mapping from whole-genome sequencing, we tested almost nine million genetic variants across the genome and identified seven risk loci, including two novel loci. One novel locus (lead single-nucleotide variant [SNV] rs12614435; p = 6.76 × 10−18) comprised intronic and several highly correlated missense variants situated in the I-, A-, and M-bands of titin, which is the largest protein in humans and responsible for the passive elasticity of heart and skeletal muscle. The other novel locus (lead SNV rs56202902; p = 1.54 × 10−11) covered a large, gene-dense chromosome 1 region that has previously been linked to cardiac conduction. Pathway and functional enrichment analyses suggested that many AF-associated genetic variants act through a mechanism of impaired muscle cell differentiation and tissue formation during fetal heart development.

Published
2018
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43. Detection of Drug-Induced Torsades de Pointes Arrhythmia Mechanisms Using hiPSC-CM Syncytial Monolayers in a High-Throughput Screening Voltage Sensitive Dye Assay.

Author

Rocha, Andre Monteiro da, Creech, Jeffery, Thonn, Ethan, Mironov, Sergey, and Herron, Todd J

Subjects
ARRHYTHMIA, ATRIAL arrhythmias, MONOMOLECULAR films, SODIUM channels, ELECTRIC potential, CONFORMANCE testing, CELL lines
Abstract

We validated 3 distinct hiPSC-CM cell lines—each of different purity and a voltage sensitive dye (VSD)-based high-throughput proarrhythmia screening assay as a noncore site in the recently completed CiPA Myocyte Phase II Validation Study. Blinded validation was performed using 12 drugs linked to low, intermediate, or high risk for causing Torsades de Pointes (TdP). Commercially sourced hiPSC-CMs were obtained either from Cellular Dynamics International (CDI, Madison, Wisconsin, iCell Cardiomyoyctes2) or Takara Bio (CLS, Cellartis Cardiomyocytes). A third hiPSC-CM cell line (MCH, Michigan) was generated in house. Each cell type had distinct baseline electrophysiological function (spontaneous beat rate, action potential duration, and conduction velocity) and drug responsiveness. Use of VSD and optical mapping enabled the detection of conduction slowing of sodium channel blockers (quinidine, disopyramide, and mexiletine) and drug-induced TdP-like activation patterns (rotors) for some high- and intermediate-risk compounds. Low-risk compounds did not induce rotors in any cell type tested. These results further validate the utility of hiPSC-CMs for predictive proarrhythmia screening and the utility of VSD technology to detect drug-induced APD prolongation, arrhythmias (rotors), and conduction slowing. Importantly, results indicate that different ratios of cardiomyocytes and noncardiomyocytes have important impact on drug response that may be considered during risk assessment of new drugs. Finally, we present the first blinded CiPA hiPSC-CM validation results to simultaneously detect drug-induced conduction slowing, action potential duration prolongation, action potential triangulation, and drug-induced rotors in a proarrhythmia assay. [ABSTRACT FROM AUTHOR]

Published
2020
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46. 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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47. 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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48. Sap97 Expression is Important for Heart Rate Control in the Murine Sinus Node

Author

Herron, Todd, primary, Rosinski, Brad, additional, Ramos Mondragon, Roberto, additional, Musa, Hassan, additional, Aoun, Kamel, additional, Mundada, Lakshmi, additional, Whitesall, Steven, additional, Chen, Yan, additional, Wang, Nulang, additional, Guerrero-Serna, Guadalupe, additional, Valdivia, Hector, additional, and Anumonwo, Justus M., additional

Published
2018
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