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3. MTORC1 regulates cardiac function and myocyte survival through 4E-BP1 inhibition in mice

Author

Zhang, Denghong, Contu, Riccardo, Latronico, Michael V.G., Zhang, Jian Ling, Rizzi, Roberto, Catalucci, Daniele, Miyamoto, Shigeki, Huang, Katherine, Ceci, Marcello, Gu, Yusu, Dalton, Nancy D., Peterson, Kirk L., Guan, Kun-Liang, Brown, Joan Heller, Chen, Ju, Sonenberg, Nahum, and Condorelli, Gianluigi

Subjects
Physiological aspects, Genetic aspects, Properties, Heart cells -- Genetic aspects -- Physiological aspects, Binding proteins -- Properties -- Physiological aspects -- Genetic aspects, Gene expression -- Physiological aspects -- Genetic aspects
Abstract

Introduction Mechanistic target of rapamycin (MTOR) is a key regulator of protein synthesis in the cardiomyocyte (1, 2). Increased protein synthesis underpins hypertrophic growth, a salient feature of the heart [...], Mechanistic target of rapamycin (MTOR) plays a critical role in the regulation of cell growth and in the response to energy state changes. Drugs inhibiting MTOR are increasingly used in antineoplastic therapies. Myocardial MTOR activity changes during hypertrophy and heart failure (HF). However, whether MTOR exerts a positive or a negative effect on myocardial function remains to be fully elucidated. Here, we show that ablation of Mtor in the adult mouse myocardium results in a fatal, dilated cardiomyopathy that is characterized by apoptosis, autophagy, altered mitochondrial structure, and accumulation of eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1). 4E-BP1 is an MTOR-containing multi-protein complex-1 (MTORC1) substrate that inhibits translation initiation. When subjected to pressure overload, Mtor-ablated mice demonstrated an impaired hypertrophic response and accelerated HF progression. When the gene encoding 4E-BP1 was ablated together with Mtor, marked improvements were observed in apoptosis, heart function, and survival. Our results demonstrate a role for the MTORC1 signaling network in the myocardial response to stress. In particular, they highlight the role of 4E-BP1 in regulating cardiomyocyte viability and in HF. Because the effects of reduced MTOR activity were mediated through increased 4E-BP1 inhibitory activity, blunting this mechanism may represent a novel therapeutic strategy for improving cardiac function in clinical HF.

Published
2010
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5. List of Contributors

Author

Allen, Paul D., primary, Amadi, Ovid C., additional, Anderson, Mark, additional, Andersson, Daniel C., additional, Archer, Stephen L., additional, Arnett, Andrea L.H., additional, Arnoldi, Richard, additional, Arrowsmith, Sarah, additional, Barton, Elisabeth R., additional, Bassel-Duby, Rhonda, additional, Belmonte, Stephen L., additional, Yaou, Rabah Ben, additional, Benjamin, Ivor J., additional, Berk, Bradford C., additional, Bers, Donald M., additional, Bertrand, Anne T., additional, Betzenhauser, Matthew J., additional, Birnbaum, Morris J., additional, Black, Brian L., additional, Blaxall, Burns C., additional, Bolli, Roberto, additional, Bonanno, Elena, additional, Bonne, Gisèle, additional, Bönnemann, Carsten G., additional, Bowens, Nina, additional, Brønnum, Hasse, additional, Bruneau, Benoit G., additional, Buckingham, Margaret, additional, Burdyga, Theodor, additional, Butler-Browne, Gillian, additional, Buttrick, Peter, additional, Cahill, P.A., additional, Calvert, John W., additional, Campbell, Kevin P., additional, Cannon, Stephen C., additional, Cattaneo, Paola, additional, Chakravarti, Aravinda, additional, Chamberlain, Jeffrey S., additional, Chaponnier, Christine, additional, Chin, Stephanie E., additional, David Cohen, Ethan, additional, Cohn, Ronald D., additional, Condorelli, Gianluigi, additional, Cummins, James H., additional, Davies, Kelvin P., additional, Deasy, Bridget, additional, DeMazumder, Deeptankar, additional, Demer, Linda, additional, de Wit, Cor, additional, Dietz, Harry C., additional, Di Lisa, Fabio, additional, DiMauro, Salvatore, additional, Dobner, Stephan, additional, Dorn, Gerald W., additional, Doroudgar, Shirin, additional, Edgerton, V. Reggie, additional, Emerson, Charles P., additional, Engel, Andrew G., additional, Esser, Karyn A., additional, Fang, Yong-Hu, additional, Feng, QiPing, additional, Fishman, Glenn I., additional, Force, Thomas, additional, Frangogiannis, Nikolaos G., additional, Franzini-Armstrong, Clara, additional, Frey, Norbert, additional, Frid, Maria G., additional, Gabbiani, Giulio, additional, Gelb, Bruce D., additional, George, Eric M., additional, Gerdes, A. Martin, additional, Gharaibeh, Burhan, additional, Gillespie, Hamilton S., additional, Glembotski, Christopher C., additional, Gori, Tommaso, additional, Granger, Joey P., additional, Griendling, Kathy K., additional, Gunst, Susan J., additional, Guttridge, Denis C., additional, Hajjar, Roger J., additional, Haller, Ronald G., additional, Hernández-Ochoa, Erick O., additional, Herring, Neil, additional, Hilenski, Lula L., additional, Hill, Joseph A., additional, Hill, Michael A., additional, Himeda, Charis L., additional, Hinz, Boris, additional, Houser, Steven R., additional, Huard, Johnny, additional, Jackson, William F., additional, Lynn Jefferies, John, additional, Kalluri, Raghu, additional, Kamal, Fadia A., additional, Kapoor, Ashish, additional, Kass, David A., additional, Katz, Arnold M., additional, Kelly, Daniel P., additional, Khakoo, Aarif Y., additional, Kharade, Sujay V., additional, Kim, Eugene, additional, Kim, Jung A., additional, Kitsis, Richard N., additional, Kobayashi, Yvonne M., additional, Komuro, Issei, additional, Kramerova, Irina, additional, Kwartler, Callie S., additional, Lakatta, Edward G., additional, Lally, Triona, additional, Larsson, Lars, additional, Latronico, Michael V.G., additional, Lavandero, Sergio, additional, Lavasani, Mitra, additional, Lee, Richard T., additional, Lee, Se-Jin, additional, il Lee, Young, additional, Lefer, David J., additional, Leinwand, Leslie A., additional, Levine, Benjamin, additional, Li, Yong, additional, Liggett, Stephen B., additional, Lin, Zhiqiang, additional, Liu, Ning, additional, Lopez, Jose R., additional, Losordo, Douglas W., additional, MacRae, Calum A., additional, Maejima, Yasuhiro, additional, Majesky, Mark W., additional, Marks, Andrew R., additional, Martin, Melissa L., additional, Mauriello, Alessandro, additional, Mayeuf, Alicia, additional, McCarthy, John J., additional, McNally, Elizabeth, additional, Meininger, Gerald A., additional, Mercola, Mark, additional, Miano, Joseph M., additional, Carrie Miceli, M., additional, Milewicz, Dianna M., additional, Morgan, Kathleen G., additional, Morrisey, Edward E., additional, Mouly, Vincent, additional, Münzel, Thomas, additional, Murphy, Anne, additional, Muslin, Anthony J., additional, Kannan Mutharasan, R., additional, Nagaraju, Kanneboyina, additional, Naito, Atsuhiko T., additional, Napolitano, Carlo, additional, Nathan, Sandeep, additional, Nozik-Grayck, Eva, additional, Ochala, Julien, additional, Offermanns, Stefan, additional, Olson, Eric N., additional, Orlandi, Augusto, additional, Papait, Roberto, additional, Parmacek, Michael S., additional, Patel, Amit R., additional, Paterson, David J., additional, Pathan, Asif R., additional, Patterson, Cam, additional, Paul, Richard J., additional, Piao, Lin, additional, Priori, Silvia G., additional, Pu, William T., additional, Ram, Rashmi, additional, Rame, J. Eduardo, additional, Ramos, Julian N., additional, Redmond, E.M., additional, Reggiani, Carlo, additional, Rich, Stuart, additional, Rinaldi, Chiara, additional, Rothermel, Beverly A., additional, Roy, Roland R., additional, Rusch, Nancy J., additional, Ryan, John J., additional, Sadoshima, Junichi, additional, San Martín, Alejandra, additional, Scarpulla, Richard C., additional, Schiaffino, Stefano, additional, Schiffrin, Ernesto L., additional, Schneider, Jay W., additional, Schneider, Martin F., additional, Schober, Andreas, additional, Scimeca, Manuel, additional, Scorrano, Luca, additional, Shih, Tiffany L., additional, Shiojima, Ichiro, additional, Siegman, Marion J., additional, Smolock, Elaine, additional, Solaro, R. John, additional, Somlyo, Avril V., additional, Sowers, James R., additional, Spagnoli, Luigi Giusto, additional, Spencer, Melissa J., additional, Spragg, David, additional, Stastna, Miroslava, additional, Steenbergen, Charles, additional, Stenmark, Kurt R., additional, Strait, James B., additional, Sweeney, H. Lee, additional, Taegtmeyer, Heinrich, additional, Takimoto, Eiki, additional, Thakali, Keshari M., additional, Thompson, Wesley J., additional, Thornton, Charles, additional, Tidball, James G., additional, Tintut, Yin, additional, Tomaselli, Gordon F., additional, Touyz, Rhian M., additional, Towbin, Jeffrey A., additional, Tsai, Kevin, additional, Vallese, Denis, additional, Van Eyk, Jennifer E., additional, Van Rooij, Eva, additional, Vetterkind, Susanne, additional, Voermans, Nicol C., additional, Volpe, Antonio, additional, Wang, Xuejun, additional, Wang, Yanggan, additional, Wang, Yibin, additional, Ware, Stephanie, additional, Weber, Christian, additional, Whaley-Connell, Adam, additional, Wilke, Russell A., additional, Wirth, Angela, additional, Wray, Susan, additional, Yada, Erica, additional, Yeager, Michael E., additional, Yutzey, Katherine E., additional, Zablocki, Daniela, additional, Zhang, Cuihua, additional, Zhang, Hanrui, additional, Zhang, Pingbo, additional, Zhe, Zhou, additional, and Zhou, Bin, additional

Published
2012
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6. Akt induces enhanced myocardial contractility and cell size in vivo in transgenic mice

Author

Condorelli, Gianluigi, Drusco, Alessandra, Stassi, Giorgio, Bellacosa, Alfonso, Roncarati, Roberta, Iaccarino, Guido, Russo, Matteo A., Gu, Yusu, Dalton, Nancy, Chung, Clarence, Latronico, Michael V.G., Napoli, Claudio, Sadoshima, Junichi, Croce, Carlo M., and Ross, John, Jr.

Subjects
Cytochemistry -- Research, Molecular biology -- Research, Heart muscle -- Physiological aspects, Genetically modified mice -- Usage, Muscle contraction -- Physiological aspects, Protein kinases -- Physiological aspects, Heart cells -- Genetic aspects, Science and technology
Abstract

The serine-threonine kinase Akt seems to be central in mediating stimuli from different classes of receptors. In fact, both IGF-1 and IL6-like cytokines induce hypertrophic and antiapoptotic signals in cardiomyocytes through PI3K-dependent Akt activation. More recently, it was shown that Akt is involved also in the hypertrophic and antiapoptotic effects of [beta]-adrenergic stimulation. Thus, to determine the effects of Akt on cardiac function in vivo, we generated a model of cardiac-specific Akt overexpression in mice. Transgenic mice were generated by using the E40K, constitutively active mutant of Akt linked to the rat [alpha]-myosin heavy chain promoter. The effects of cardiac-selective Akt overexpression were studied by echocardiography, cardiac catheterization, histological and biochemical techniques. We found that Akt overexpression produced cardiac hypertrophy at the molecular and histological levels, with a significant increase in cardiomyocyte cell size and concentric LV hypertrophy. Akt-transgenic mice also showed a remarkable increase in cardiac contractility compared with wild-type controls as demonstrated by the analysis of left ventricular ([dP/dt.sub.max]) in an invasive hemodynamic study, although with graded dobutamine infusion, the maximum response was not different from that in controls. Diastolic function, evaluated by left ventricular [dP/dt.sub.min], was not affected at rest but was impaired during graded dobutamine infusion. Isoproterenol-induced cAMP levels, [beta]-adrenergic receptor ([beta]-AR) density, and [beta]-AR affinity were not altered compared with control mice. Moreover, studies on signaling pathway activation from myocardial extracts demonstrated that glycogen synthase kinase3-[beta] is phosphorylated, whereas p42/44 mitogen--activated protein kinases is not, indicating that Akt induces hypertrophy in vivo by activating the glycogen synthase kinase3-[beta]/GATA 4 pathway. In summary, our results not only demonstrate that Akt regulates cardiomyocyte cell size in vivo, but, importantly, show that Akt modulates cardiac contractility in vivo without directly affecting [beta]-AR signaling capacity.

Published
2002

10. microRNAs in cardiovascular diseases: current knowledge and the road ahead

Author

Condorelli, Gianluigi, Latronico, Michael V.G., and Cavarretta, Elena

Subjects
MicroRNAs, microRNA, cardiovascular disease, Cardiovascular Diseases, microRNAs, cardiovascular diseases, hypertrophic cardiomyopathy, Animals, Humans, heart disease, Genetic Therapy
Abstract

Over the last few years, the field of microribonucleic acid (miRNA) in cardiovascular biology and disease has expanded at an incredible pace. miRNAs are themselves part of a larger family, that of non-coding RNAs, the importance of which for biological processes is starting to emerge. miRNAs are ∼22-nucleotide-long RNA sequences that can legate messenger (m)RNAs at partially complementary binding sites, and hence regulate the rate of protein synthesis by altering the stability of the targeted mRNAs. In the cardiovascular system, miRNAs have been shown to be critical regulators of development and physiology. They control basic functions in virtually all cell types relevant to the cardiovascular system (such as endothelial cells, cardiac muscle, smooth muscle, inflammatory cells, and fibroblasts) and, thus, are directly involved in the pathophysiology of many cardiovascular diseases. As a result of their role in disease, they are being studied for exploitation in diagnostics, prognostics, and therapeutics. However, there are still significant obstacles that need to be overcome before they enter the clinical arena. We present here a review of the literature and outline the directions toward their use in the clinic.

Published
2013

14. Reply

Author

Viviani Anselmi, Chiara, primary, Briguori, Carlo, additional, Roncarati, Roberta, additional, Papa, Laura, additional, Visconti, Gabriella, additional, Focaccio, Amelia, additional, De Micco, Francesca, additional, Latronico, Michael V.G., additional, Pagnotta, Paolo, additional, and Condorelli, Gianluigi, additional

Published
2014
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15. Circulating miR-29a, Among Other Up-Regulated MicroRNAs, Is the Only Biomarker for Both Hypertrophy and Fibrosis in Patients With Hypertrophic Cardiomyopathy

Author

Roncarati, Roberta, primary, Viviani Anselmi, Chiara, additional, Losi, Maria Angela, additional, Papa, Laura, additional, Cavarretta, Elena, additional, Da Costa Martins, Paula, additional, Contaldi, Carla, additional, Saccani Jotti, Gloria, additional, Franzone, Anna, additional, Galastri, Laura, additional, Latronico, Michael V.G., additional, Imbriaco, Massimo, additional, Esposito, Giovanni, additional, De Windt, Leon, additional, Betocchi, Sandro, additional, and Condorelli, Gianluigi, additional

Published
2014
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16. Routine Assessment of On-Clopidogrel Platelet Reactivity and Gene Polymorphisms in Predicting Clinical Outcome Following Drug-Eluting Stent Implantation in Patients With Stable Coronary Artery Disease

Author

Viviani Anselmi, Chiara, primary, Briguori, Carlo, additional, Roncarati, Roberta, additional, Papa, Laura, additional, Visconti, Gabriella, additional, Focaccio, Amelia, additional, De Micco, Francesca, additional, Latronico, Michael V.G., additional, Pagnotta, Paolo, additional, and Condorelli, Gianluigi, additional

Published
2013
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20. Unexpectedly low mutation rates in beta‐myosin heavy chain and cardiac myosin binding protein genes in italian patients with hypertrophic cardiomyopathy

Author

Roncarati, Roberta, primary, Latronico, Michael V.G., additional, Musumeci, Beatrice, additional, Aurino, Stefania, additional, Torella, Annalaura, additional, Bang, Marie‐Louise, additional, Jotti, Gloria Saccani, additional, Puca, Annibale A., additional, Volpe, Massimo, additional, Nigro, Vincenzo, additional, Autore, Camillo, additional, and Condorelli, Gianluigi, additional

Published
2011
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24. Isolation and Expansion of Adult Cardiac Stem Cells From Human and Murine Heart

Author

Messina, Elisa, primary, De Angelis, Luciana, additional, Frati, Giacomo, additional, Morrone, Stefania, additional, Chimenti, Stefano, additional, Fiordaliso, Fabio, additional, Salio, Monica, additional, Battaglia, Massimo, additional, Latronico, Michael V.G., additional, Coletta, Marcello, additional, Vivarelli, Elisabetta, additional, Frati, Luigi, additional, Cossu, Giulio, additional, and Giacomello, Alessandro, additional

Published
2004
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28. A collagen membrane-based engineered heart tissue improves cardiac function in ischemic rat hearts

Author

Latronico, Michael V.G., Tampieri, Anna, Condorelli, Gianluigi, Levialdi Ghiron, Jung Hee, Esposito, Giovanni, Schiattarella, Gabriele G., Chiariello, Giovanni A., Sandri, Monica, Rizzi, Roberto, and Pironti, Gianluigi

Abstract

In the relatively new field of cardiac tissue engineering, different biomaterials, methods and techniques have been tested for cardiac repair, but we are still far from the achievement of a valid model that can be tested for therapeutic goals. In this study, the authors examined the efficacy of newly preformed membranes based on collagen type I for the transplantation of cardiac cells. The membrane prototype, cross-linked with 1,4-butanediol diglycidyl ether (BDDGE) and fibronectin-enriched, gave rise to spontaneously beating heart cell constructs, 5–9 days after seeding with neonatal rat cardiac cells. This membrane was grafted, with and without beating cardiac cells, onto the infarcted area of rat models of heart failure. Seriate echocardiography, performed on rats before transplantation and at 4 and 8 weeks after transplantation, demonstrated that rats treated with collagen membranes previously seeded with beating cells showed an improvement in cardiac function after 8 weeks. These results suggest that this new type of collagen membrane can be used as vector for the transplantation of beating heart cells for the regeneration of the injured myocardium and hence represents an important potential tool for cardiac tissue repair technologies.In the relatively young field of cardiac tissue engineering, different biomaterials, methods and techniques have been tested for cardiac repair, but we are still far from the achievement of a valid model that can be tested for therapeutic goals. In this study we examined the efficacy of new preformed membranes based on collagen type I for the transplantation of cardiac cells. The membrane prototype, cross-linked with 1,4-butanediol diglycidyl ether (BDDGE) and fibronectin-enriched, gave rise to spontaneously beating heart cell constructs 5–9 days after seeding with neonatal rat cardiac cells. This membrane was grafted, with and without beating cardiac cells, onto the infarcted area of rat models of heart failure. Seriate echocardiography, performed on rats before transplantation and at 4 and 8 weeks after transplantation, demonstrated that rats treated with collagen membranes previously seeded with beating cells showed an improvement in cardiac function after 8 weeks. These results suggest that this new type of collagen membrane can be used as vector for the transplantation of beating heart cells for the regeneration of the injured myocardium and hence represents an important potential tool for cardiac tissue repair technologies.

Published
2013
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