Search

Your search keyword '"Rabinowitz, Joseph"' showing total 493 results
Start Over Author "Rabinowitz, Joseph"
493 results on '"Rabinowitz, Joseph"'

3. Nuclear translocation of cardiac G protein-Coupled Receptor kinase 5 downstream of select Gq-activating hypertrophic ligands is a calmodulin-dependent process.

Author

Gold, Jessica I, Martini, Jeffrey S, Hullmann, Jonathan, Gao, Erhe, Chuprun, J Kurt, Lee, Linda, Tilley, Douglas G, Rabinowitz, Joseph E, Bossuyt, Julie, Bers, Donald M, and Koch, Walter J

Subjects
Myocardium, Cell Membrane, Cell Nucleus, Animals, Mice, Transgenic, Rabbits, Mice, Rats, Adenoviridae, Hypertrophy, Phenylephrine, GTP-Binding Protein alpha Subunits, Gq-G11, Angiotensin II, Calmodulin, Ligands, Gene Expression Regulation, Enzymologic, Protein Structure, Tertiary, Protein Binding, Active Transport, Cell Nucleus, Male, G-Protein-Coupled Receptor Kinase 5, Active Transport, GTP-Binding Protein alpha Subunits, Gq-G11, Gene Expression Regulation, Enzymologic, Transgenic, Protein Structure, Tertiary, General Science & Technology
Abstract

G protein-Coupled Receptors (GPCRs) kinases (GRKs) play a crucial role in regulating cardiac hypertrophy. Recent data from our lab has shown that, following ventricular pressure overload, GRK5, a primary cardiac GRK, facilitates maladaptive myocyte growth via novel nuclear localization. In the nucleus, GRK5's newly discovered kinase activity on histone deacetylase 5 induces hypertrophic gene transcription. The mechanisms governing the nuclear targeting of GRK5 are unknown. We report here that GRK5 nuclear accumulation is dependent on Ca(2+)/calmodulin (CaM) binding to a specific site within the amino terminus of GRK5 and this interaction occurs after selective activation of hypertrophic Gq-coupled receptors. Stimulation of myocytes with phenylephrine or angiotensinII causes GRK5 to leave the sarcolemmal membrane and accumulate in the nucleus, while the endothelin-1 does not cause nuclear GRK5 localization. A mutation within the amino-terminus of GRK5 negating CaM binding attenuates GRK5 movement from the sarcolemma to the nucleus and, importantly, overexpression of this mutant does not facilitate cardiac hypertrophy and related gene transcription in vitro and in vivo. Our data reveal that CaM binding to GRK5 is a physiologically relevant event that is absolutely required for nuclear GRK5 localization downstream of hypertrophic stimuli, thus facilitating GRK5-dependent regulation of maladaptive hypertrophy.

Published
2013

5. Adeno-Associated Virus Serotype 9–Driven Expression of BAG3 Improves Left Ventricular Function in Murine Hearts With Left Ventricular Dysfunction Secondary to a Myocardial Infarction

Author

Knezevic, Tijana, Myers, Valerie D., Su, Feifei, Wang, JuFang, Song, Jianliang, Zhang, Xue-Qian, Gao, Erhe, Gao, Guofeng, Madesh, Muniswamy, Gupta, Manish K., Gordon, Jennifer, Weiner, Kristen N., Rabinowitz, Joseph, Ramsey, Frederick V., Tilley, Douglas G., Khalili, Kamel, Cheung, Joseph Y., and Feldman, Arthur M.

Published
2016
Full Text
View/download PDF

15. A comprehensive study of a 29-capsid AAV library in a non-human primate central nervous system

Author

Kondratov, Oleksandr, primary, Kondratova, Liudmyla, additional, Mandel, Ronald J., additional, Coleman, Kirsten, additional, Savage, Michael A., additional, Gray-Edwards, Heather L., additional, Ness, Timothy J., additional, Rodriguez-Lebron, Edgar, additional, Bell, Robert D., additional, Rabinowitz, Joseph, additional, Gamlin, Paul D., additional, and Zolotukhin, Sergei, additional

Published
2021
Full Text
View/download PDF

17. CpG-depleted adeno-associated virus vectors evade immune detection

Author

Faust, Susan M., Bell, Peter, Cutler, Benjamin J., Ashley, Scott N., Zhu, Yanqing, Rabinowitz, Joseph E., and Wilson, James M.

Subjects
Viral genetics -- Research, Dependoviruses -- Research, Genetic vectors -- Research, Health care industry
Abstract

Due to their efficient transduction potential, adeno-associated virus (AAV) vectors are leading candidates for gene therapy in skeletal muscle diseases. However, immune responses toward the vector or transgene product have [...]

Published
2013
Full Text
View/download PDF

22. Remodeling of cortical bone allografts mediated by adherent rAAV-RANKL and VEGF gene therapy

Author

Ito, Hiromu, Koefoed, Mette, Tiyapatanaputi, Prarop, Gromov, Kirill, Goater, J Jeffrey, Carmouche, Jonathan, Zhang, Xinping, Rubery, Paul T, Rabinowitz, Joseph, Samulski, R Jude, Nakamura, Takashi, Soballe, Kjeld, O'Keefe, Regis J, Boyce, Brendan F, and Schwarz, Edward M

Abstract

Structural allograft healing is limited because of a lack of vascularization and remodeling. To study this we developed a mouse model that recapitulates the clinical aspects of live autograft and processed allograft healing. Gene expression analyses showed that there is a substantial decrease in the genes encoding RANKL and VEGF during allograft healing. Loss-of-function studies showed that both factors are required for autograft healing. To determine whether addition of these signals could stimulate allograft vascularization and remodeling, we developed a new approach in which rAAV can be freeze-dried onto the cortical surface without losing infectivity. We show that combination rAAV-RANKL- and rAAV-VEGF-coated allografts show marked remodeling and vascularization, which leads to a new bone collar around the graft. In conclusion, we find that RANKL and VEGF are necessary and sufficient for efficient autograft remodeling and can be transferred using rAAV to revitalize structural allografts., Author(s): Hiromu Ito [1, 2]; Mette Koefoed [1, 3]; Prarop Tiyapatanaputi [1]; Kirill Gromov [1, 3]; J Jeffrey Goater [1]; Jonathan Carmouche [1]; Xinping Zhang [1]; Paul T Rubery [1]; [...]

Published
2005
Full Text
View/download PDF

32. Converging Mechanisms of p53 Activation Drive Motor Neuron Degeneration in Spinal Muscular Atrophy

Author

Simon, Christian M., primary, Dai, Ya, additional, Van Alstyne, Meaghan, additional, Koutsioumpa, Charalampia, additional, Pagiazitis, John G., additional, Chalif, Joshua I., additional, Wang, Xiaojian, additional, Rabinowitz, Joseph E., additional, Henderson, Christopher E., additional, Pellizzoni, Livio, additional, and Mentis, George Z., additional

Published
2017
Full Text
View/download PDF

38. Abstract 298: Circular Rna Mmu_circ_008396 Attenuates Cardiac Remodeling After Myocardial Infarction in Mice

Author

Garikipati, Venkata N, primary, Verma, Suresh K, additional, Cheng, Zhongjian, additional, Trungcao, May M, additional, Liang, Dongming, additional, Khan, Mohsin, additional, Benedict, Cindy, additional, Cimini, Maria, additional, Ibetti, Jessica, additional, Grisanti, Laurel, additional, Schumacher, Sarah M, additional, Gao, Erhe, additional, Rabinowitz, Joseph E, additional, Wilusz, Jeremy E, additional, Goukassian, David, additional, Houser, Steven, additional, Koch, Walter J, additional, and Kishore, Raj, additional

Published
2017
Full Text
View/download PDF

39. Cardiac Dysfunction in HIV‐1 Transgenic Mouse: Role of Stress and BAG3

Author

Cheung, Joseph Y., Gordon, Jennifer, Wang, JuFang, Song, Jianliang, Zhang, Xue‐Qian, Tilley, Douglas G., Gao, Erhe, Koch, Walter J., Rabinowitz, Joseph, Klotman, Paul E., Khalili, Kamel, and Feldman, Arthur M.

Subjects
Mice, Inbred C57BL, Acquired Immunodeficiency Syndrome, Mice, Stress, Physiological, Original Research Articles, HIV-1, Animals, Mice, Transgenic, Apoptosis Regulatory Proteins, Cardiomyopathies, Myocardial Contraction, Adaptor Proteins, Signal Transducing
Abstract

Since highly active antiretroviral therapy improved long-term survival of acquired immunodeficiency syndrome (AIDS) patients, AIDS cardiomyopathy has become an increasingly relevant clinical problem. We used human immunodeficiency virus (HIV)-1 transgenic (Tg26) mouse to explore molecular mechanisms of AIDS cardiomyopathy. Tg26 mice had significantly lower left ventricular (LV) mass and smaller end-diastolic and end-systolic LV volumes. Under basal conditions, cardiac contractility and relaxation and single myocyte contraction dynamics were not different between wild-type (WT) and Tg26 mice. Ten days after open heart surgery, contractility and relaxation remained significantly depressed in Tg26 hearts, suggesting that Tg26 mice did not tolerate surgical stress well. To simulate heart failure in which expression of Bcl2-associated athanogene 3 (BAG3) is reduced, we down-regulated BAG3 by small hairpin ribonucleic acid in WT and Tg26 hearts. BAG3 down-regulation significantly reduced contractility in Tg26 hearts. BAG3 overexpression rescued contractile abnormalities in myocytes expressing the HIV-1 protein Tat. We conclude: (i) Tg26 mice exhibit normal contractile function at baseline; (ii) Tg26 mice do not tolerate surgical stress well; (iii) BAG3 down-regulation exacerbated cardiac dysfunction in Tg26 mice; (iv) BAG3 overexpression rescued contractile abnormalities in myocytes expressing HIV-1 protein Tat; and (v) BAG3 may occupy a role in pathogenesis of AIDS cardiomyopathy.

Published
2015

40. Bcl-2–associated athanogene 3 protects the heart from ischemia/reperfusion injury

Author

Su, Feifei, primary, Myers, Valerie D., additional, Knezevic, Tijana, additional, Wang, JuFang, additional, Gao, Erhe, additional, Madesh, Muniswamy, additional, Tahrir, Farzaneh G., additional, Gupta, Manish K., additional, Gordon, Jennifer, additional, Rabinowitz, Joseph, additional, Ramsey, Frederick V., additional, Tilley, Douglas G., additional, Khalili, Kamel, additional, Cheung, Joseph Y., additional, and Feldman, Arthur M., additional

Published
2016
Full Text
View/download PDF

41. Restoration of Hydrogen Sulfide Production in Diabetic Mice Improves Reparative Function of Bone Marrow Cells

Author

Cheng, Zhongjian, primary, Garikipati, Venkata Naga Srikanth, additional, Nickoloff, Emily, additional, Wang, Chunlin, additional, Polhemus, David J., additional, Zhou, Jibin, additional, Benedict, Cynthia, additional, Khan, Mohsin, additional, Verma, Suresh K., additional, Rabinowitz, Joseph E., additional, Lefer, David, additional, and Kishore, Raj, additional

Published
2016
Full Text
View/download PDF

42. Thrombospondin expression in myofibers stabilizes muscle membranes

Author

Vanhoutte, Davy, primary, Schips, Tobias G, additional, Kwong, Jennifer Q, additional, Davis, Jennifer, additional, Tjondrokoesoemo, Andoria, additional, Brody, Matthew J, additional, Sargent, Michelle A, additional, Kanisicak, Onur, additional, Yi, Hong, additional, Gao, Quan Q, additional, Rabinowitz, Joseph E, additional, Volk, Talila, additional, McNally, Elizabeth M, additional, and Molkentin, Jeffery D, additional

Published
2016
Full Text
View/download PDF

43. Author response: Thrombospondin expression in myofibers stabilizes muscle membranes

Author

Vanhoutte, Davy, primary, Schips, Tobias G, additional, Kwong, Jennifer Q, additional, Davis, Jennifer, additional, Tjondrokoesoemo, Andoria, additional, Brody, Matthew J, additional, Sargent, Michelle A, additional, Kanisicak, Onur, additional, Yi, Hong, additional, Gao, Quan Q, additional, Rabinowitz, Joseph E, additional, Volk, Talila, additional, McNally, Elizabeth M, additional, and Molkentin, Jeffery D, additional

Published
2016
Full Text
View/download PDF

44. Abstract 24: Hydrogen Sulfide Potentiates Bone Marrow-derived Angiogenic Progenitor Cell-mediated Ischemic Limb Angiogenesis in Diabetic Animals

Author

Cheng, Zhongjian, primary, Garikipati, Venkata NS, additional, Nickoloff, Emily, additional, Wang, Chunlin, additional, Polhemus, David, additional, Zhou, Jibin, additional, Benedict, Cynthia, additional, Verma, Suresh K, additional, Khan, Mohsin, additional, Rabinowitz, Joseph E, additional, Lefer, David, additional, and Kishore, Raj, additional

Published
2016
Full Text
View/download PDF

45. Leukocyte-Expressed β 2 -Adrenergic Receptors Are Essential for Survival After Acute Myocardial Injury

Author

Grisanti, Laurel A., primary, Gumpert, Anna M., additional, Traynham, Christopher J., additional, Gorsky, Joshua E., additional, Repas, Ashley A., additional, Gao, Erhe, additional, Carter, Rhonda L., additional, Yu, Daohai, additional, Calvert, John W., additional, García, Andrés Pun, additional, Ibáñez, Borja, additional, Rabinowitz, Joseph E., additional, Koch, Walter J., additional, and Tilley, Douglas G., additional

Published
2016
Full Text
View/download PDF

46. MCUR1 Is a Scaffold Factor for the MCU Complex Function and Promotes Mitochondrial Bioenergetics

Author

Tomar, Dhanendra, primary, Dong, Zhiwei, additional, Shanmughapriya, Santhanam, additional, Koch, Diana A., additional, Thomas, Toby, additional, Hoffman, Nicholas E., additional, Timbalia, Shrishiv A., additional, Goldman, Samuel J., additional, Breves, Sarah L., additional, Corbally, Daniel P., additional, Nemani, Neeharika, additional, Fairweather, Joseph P., additional, Cutri, Allison R., additional, Zhang, Xueqian, additional, Song, Jianliang, additional, Jaña, Fabián, additional, Huang, Jianhe, additional, Barrero, Carlos, additional, Rabinowitz, Joseph E., additional, Luongo, Timothy S., additional, Schumacher, Sarah M., additional, Rockman, Michael E., additional, Dietrich, Alexander, additional, Merali, Salim, additional, Caplan, Jeffrey, additional, Stathopulos, Peter, additional, Ahima, Rexford S., additional, Cheung, Joseph Y., additional, Houser, Steven R., additional, Koch, Walter J., additional, Patel, Vickas, additional, Gohil, Vishal M., additional, Elrod, John W., additional, Rajan, Sudarsan, additional, and Madesh, Muniswamy, additional

Published
2016
Full Text
View/download PDF

48. BAG3 regulates contractility and Ca2+ homeostasis in adult mouse ventricular myocytes

Author

Feldman, Arthur M., primary, Gordon, Jennifer, additional, Wang, JuFang, additional, Song, Jianliang, additional, Zhang, Xue-Qian, additional, Myers, Valerie D., additional, Tilley, Douglas G., additional, Gao, Erhe, additional, Hoffman, Nicholas E., additional, Tomar, Dhanendra, additional, Madesh, Muniswamy, additional, Rabinowitz, Joseph, additional, Koch, Walter J., additional, Su, Feifei, additional, Khalili, Kamel, additional, and Cheung, Joseph Y., additional

Published
2016
Full Text
View/download PDF

49. β1-Adrenergic Receptor and Sphingosine-1-Phosphate Receptor 1 Reciprocal Down-Regulation Influences Cardiac Hypertrophic Response and Progression Toward Heart Failure: Protective Role of S1PR1 Cardiac Gene Therapy

Author

Cannavo, Alessandro, Rengo, Giuseppe, Liccardo, Daniela, Pagano, Gennaro, Zincarelli, Carmela, De Angelis, Maria Carmen, Puglia, Roberto, Di Pietro, Elisa, Rabinowitz, Joseph E., Barone, Maria Vittoria, Cirillo, Plinio, Trimarco, Bruno, Palmer, Timothy M., Ferrara, Nicola, Koch, Walter J., Leosco, Dario, and Rapacciuolo, Antonio

Subjects
Heart Failure, Male, Green Fluorescent Proteins, Myocardial Infarction, Down-Regulation, Cardiomegaly, Genetic Therapy, Receptor Cross-Talk, Rats, Inbred WKY, Article, Rats, Mice, Inbred C57BL, Disease Models, Animal, Mice, Receptors, Lysosphingolipid, HEK293 Cells, Disease Progression, Animals, Humans, Receptors, Adrenergic, beta-1, Sphingosine-1-Phosphate Receptors, Myoblasts, Cardiac
Abstract

The sphingosine-1-phosphate receptor 1 (S1PR1) and β1-adrenergic receptor (β1AR) are G-protein-coupled receptors expressed in the heart. These 2 receptors have opposing actions on adenylyl cyclase because of differential G-protein coupling. Importantly, both of these receptors can be regulated by the actions of G-protein-coupled receptor kinase-2, which triggers desensitization and downregulation processes. Although classic signaling paradigms suggest that simultaneous activation of β1ARs and S1PR1s in a myocyte would simply result in opposing action on cAMP production, in this report we have uncovered a direct interaction between these 2 receptors, with regulatory involvement of G-protein-coupled receptor kinase-2.In HEK (human embryonic kidney) 293 cells overexpressing both β1AR and S1PR1, we demonstrated that β1AR downregulation can occur after stimulation with sphingosine-1-phosphate (an S1PR1 agonist), whereas S1PR1 downregulation can be triggered by isoproterenol (a β-adrenergic receptor agonist) treatment. This cross talk between these 2 distinct G-protein-coupled receptors appears to have physiological significance, because they interact and show reciprocal regulation in mouse hearts undergoing chronic β-adrenergic receptor stimulation and in a rat model of postischemic heart failure.We demonstrate that restoration of cardiac plasma membrane levels of S1PR1 produces beneficial effects that counterbalance the deleterious β1AR overstimulation in heart failure.

Published
2013

Catalog

Books, media, physical & digital resources
See catalog results