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102. Caveolin-3 KO Disrupts T-Tububle Structure and Decreases T-Tubular ICa Density in Mouse Ventricular Myocytes

Author

Bryant, Simon, Kong, Cherrie, Watson, Judy, Gadeberg, Hanne, Roth, David M., Patel, Hemal, Cannell, Mark, James, Andrew, and Orchard, Clive

Subjects
cardiovascular system, calcium transient, calcium current, cavolin-3, calcium release
Abstract

Caveolin-3 (Cav-3) is a protein that has been implicated in t-tubule formation and function in cardiac ventricular myocytes. In cardiac hypertrophy and failure, Cav-3 expression decreases, t-tubule structure is disrupted and excitation-contraction coupling (ECC) is impaired. However, the extent to which the decrease in Cav-3 expression underlies these changes is unclear. We therefore investigated the structure and function of myocytes isolated from the hearts of Cav-3 KO mice. These mice showed cardiac dilatation and decreased ejection fraction in vivo, compared to WT controls. Isolated KO myocytes showed cellular hypertrophy and altered t-tubule structure, and decreased L-type Ca channel (LTCC) current (ICa) density. This decrease in density occurred predominantly in the t-tubules, with no change in total ICa, and was therefore a consequence of the increase in membrane area. Cav-3 KO had no effect on LTCC expression, and C3SD peptide, which mimics the scaffolding domain of Cav-3, had no effect on ICa in KO myocytes. However, inhibiting protein kinase A using H-89 decreased ICa at the surface and t-tubule membranes in both KO and WT myocytes. Cav-3 KO had no significant effect on INCX or Ca release. These data suggest that Cav-3 KO causes cellular hypertrophy thereby decreasing t-tubular ICa density. (200 words)

Published
2018
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103. The Effects of Aging on the Regulation of T-Tubular i Ca by Caveolin in Mouse Ventricular Myocytes

Author

Kong, Cherrie H.T., Bryant, Simon M., Watson, Judy J., Gadeberg, Hanne C., Roth, David M., Patel, Hemal H., Cannell, Mark B., Orchard, Clive H., and James, Andrew F.

Subjects
Ca signaling, Caveolin-3, Excitation-contraction coupling
Abstract

Aging is associated with diminished cardiac function in males. Cardiac excitation-contraction coupling in ventricular myocytes involves Ca influx via the Ca current (I Ca) and Ca release from the sarcoplasmic reticulum, which occur predominantly at t-tubules. Caveolin-3 regulates t-tubular I Ca, partly through protein kinase A (PKA), and both I Ca and caveolin-3 decrease with age. We therefore investigated I Ca and t-tubule structure and function in cardiomyocytes from male wild-type (WT) and caveolin-3-overexpressing (Cav-3OE) mice at 3 and 24 months of age. In WT cardiomyocytes, t-tubular I Ca -density was reduced by ∼50% with age while surface I Ca density was unchanged. Although regulation by PKA was unaffected by age, inhibition of caveolin-3-binding reduced t-tubular I Ca at 3 months, but not at 24 months. While Cav-3OE increased cardiac caveolin-3 protein expression ∼2.5-fold at both ages, the age-dependent reduction in caveolin-3 (WT ∼35%) was preserved in transgenic mice. Overexpression of caveolin-3 reduced t-tubular I Ca density at 3 months but prevented further I Ca loss with age. Measurement of Ca release at the t-tubules revealed that the triggering of local Ca release by t-tubular I Ca was unaffected by age. In conclusion, the data suggest that the reduction in I Ca density with age is associated with the loss of a caveolin-3-dependent mechanism that augments t-tubular I Ca density.

Published
2018
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108. Neuron‐targeted caveolin‐1 improves neuromuscular function and extends survival in SOD1 G93A mice

Author

Sawada, Atsushi, primary, Wang, Shanshan, additional, Jian, Minyu, additional, Leem, Joseph, additional, Wackerbarth, Jesse, additional, Egawa, Junji, additional, Schilling, Jan M., additional, Platoshyn, Oleksandr, additional, Zemljic-Harpf, Alice, additional, Roth, David M., additional, Patel, Hemal H., additional, Patel, Piyush M., additional, Marsala, Martin, additional, and Head, Brian P., additional

Published
2019
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112. Haunting hues of silence

Author

Roth, David M.

Subjects
Artists, Argentine -- Works, Prints -- Evaluation, Humanities, International relations, Political science, Evaluation, Works
Abstract

Though Claudia Bernardi has never been tortured, threatened with death, or forced to witness the atrocities of warring guerrilla armies, she knows more about the lives of those who have [...]

Published
1995

114. For the birds

Author

Roth, David M.

Subjects
Farallon National Wildlife Refuge, California -- Personal narratives, Wildlife refuges -- California, Bird watching -- Personal narratives, Travel, recreation and leisure
Abstract

A day-long bird-watching trip to the Farallon Islands, 27 miles west of the Golden Gate Bridge, is described. The trip, sponsored by the Oceanic Society, gives passengers the chance to see porpoises, whales, seals and exotic fish, in addition to the seabirds.

Published
1992

115. Going Latin in Manhattan

Author

Roth, David M.

Subjects
Salsa -- New York, Travel, recreation and leisure
Abstract

The salsa nightclubs of Manhattan, NY, are noted. Though it has been around since the 1930s, only recently has salsa reached a wide audience.

Published
1992

116. Protective role of cardiac-specific overexpression of caveolin-3 in cirrhotic cardiomyopathy.

Author

So Yeon Kim, Kang Ho Kim, Schilling, Jan M., Leem, Joseph, Dhanani, Mehul, Head, Brian P., Roth, David M., Zemljic-Harpf, Alice E., and Patel, Hemal H.

Abstract

Cirrhotic cardiomyopathy is a clinical syndrome in patients with liver cirrhosis characterized by blunted cardiac contractile responses to stress and/or heart rate-corrected QT (QTc) interval prolongation. Caveolin-3 (Cav-3) plays a critical role in cardiac protection and is an emerging therapeutic target for heart disease. We investigated the protective role of cardiac-specific overexpression (OE) of Cav-3 in cirrhotic cardiomyopathy. Biliary fibrosis was induced in male Cav-3 OE mice and transgene negative (TGneg) littermates by feeding a diet containing 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC; 0.1%) for 3 wk. Liver pathology and blood chemistries were assessed, and stress echocardiography, telemetry, and isolated heart perfusion studies to assess adrenergic responsiveness were performed. Cav-3 OE mice showed a similar degree of hyperdynamic contractility, pulmonary hypertension, and QTc interval prolongation as TGneg mice after 3 wk of DDC diet. Blunted systolic responses were shown in both DDC-fed Cav-3 OE and TGneg hearts after in vivo isoproterenol challenge. However, QTc interval prolongation after in vivo isoproterenol challenge was significantly less in DDC-fed Cav-3 OE hearts compared with DDC-fed TGneg hearts. In ex vivo perfused hearts, where circulatory factors are absent, isoproterenol challenge showed hearts from DDC-fed Cav-3 OE mice had better cardiac contractility and relaxation compared with DDC-fed TGneg hearts. Although Cav-3 OE in the heart did not prevent cardiac alterations in DDC-induced biliary fibrosis, cardiac expression of Cav-3 reduced QTc interval prolongation after adrenergic stimulation in cirrhosis. NEW & NOTEWORTHY Prevalence of cirrhotic cardiomyopathy is up to 50% in cirrhotic patients, and liver transplantation is the only treatment. However, cirrhotic cardiomyopathy is associated with perioperative morbidity and mortality after liver transplantation; therefore, management of cirrhotic cardiomyopathy is crucial for successful liver transplantation. This study shows cardiac myocyte specific overexpression of caveolin-3 (Cav-3) provides better cardiac contractile responses and less corrected QT prolongation during adrenergic stress in a cirrhotic cardiomyopathy model, suggesting beneficial effects of Cav-3 expression in cirrhotic cardiomyopathy. [ABSTRACT FROM AUTHOR]

Published
2020
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118. Atorvastatin, but not pravastatin, inhibits cardiac Akt/mTOR signaling and disturbs mitochondrial ultrastructure in cardiac myocytes

Author

Godoy, Joseph C., primary, Niesman, Ingrid R., additional, Busija, Anna R., additional, Kassan, Adam, additional, Schilling, Jan M., additional, Schwarz, Anna, additional, Alvarez, Erika A., additional, Dalton, Nancy D., additional, Drummond, John C., additional, Roth, David M., additional, Kararigas, Georgios, additional, Patel, Hemal H., additional, and Zemljic-Harpf, Alice E., additional

Published
2018
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122. Chronic β1-adrenoceptor blockade impairs ischaemic tolerance and preconditioning in murine myocardium

Author

See Hoe, Louise E, Schilling, Jan M, Busija, Anna R, Haushalter, Kristofer J, Ozberk, Victoria, Keshwani, Malik M, Roth, David M, Toit, Eugene Du, Headrick, John P, Patel, Hemal H, and Peart, Jason N

Subjects
Male, Artificial Intelligence and Image Processing, beta-Adrenoceptors, Myocardial Reperfusion Injury, beta-1, Inbred C57BL, Cardiovascular, Behavioral Science & Comparative Psychology, Dose-Response Relationship, Ischaemia-reperfusion injury, Mice, Cardiovascular drugs, Heart Rate, Receptors, Animals, Myocardial, 2.1 Biological and endogenous factors, Psychology, Pharmacology & Pharmacy, Aetiology, Ischemic Preconditioning, Heart Disease - Coronary Heart Disease, L-Lactate Dehydrogenase, Morphine, Myocardium, Isoproterenol, Cardiac ischaemia, Pharmacology and Pharmaceutical Sciences, Adrenergic beta-1 Receptor Antagonists, β-Adrenoceptors, Heart Disease, Adrenergic, Cognitive Sciences, Drug
Abstract

β-adrenoceptor antagonists are commonly used in ischaemic heart disease (IHD) patients, yet may impair signalling and efficacy of 'cardioprotective' interventions. We assessed effects of chronic β1-adrenoceptor antagonism on myocardial resistance to ischaemia-reperfusion (IR) injury and the ability of cardioprotective interventions [classic ischaemic preconditioning (IPC); novel sustained ligand-activated preconditioning (SLP)] to reduce IR injury in murine hearts. Young male C57Bl/6 mice were untreated or received atenolol (0.5g/l in drinking water) for 4 weeks. Subsequently, two cardioprotective stimuli were evaluated: morphine pellets implanted (to induce SLP, controls received placebo) 5 days prior to Langendorff heart perfusion, and IPC in perfused hearts (3×1.5min ischaemia/2min reperfusion). Atenolol significantly reduced in vivo heart rate. Untreated control hearts exhibited substantial left ventricular dysfunction (~50% pressure development recovery, ~20mmHg diastolic pressure rise) with significant release of lactate dehydrogenase (LDH, tissue injury indicator) after 25min ischaemia/45min reperfusion. Contractile dysfunction and elevated LDH were reduced >50% with IPC and SLP. While atenolol treatment did not modify baseline contractile function, post-ischaemic function was significantly depressed compared to untreated hearts. Atenolol pre-treatment abolished beneficial effects of IPC, whereas SLP protection was preserved. These data indicate that chronic β1-adrenoceptor blockade can exert negative effects on functional IR tolerance and negate conventional IPC (implicating β1-adrenoceptors in IR injury and IPC signalling). However, novel morphine-induced SLP is resistant to inhibition by β1-adrenoceptor antagonism.

Published
2016

123. Colaboradores

Author

Akhtar, Shamsuddin, Armour, Sarah, Auger, William R., Augoustides, John G.T., Badescu, Gina C., Bailey, James M., Bainbridge, Daniel, Banks, Dalia A., Bansal, Manish, Barash, Paul G., Baum, Victor C., Bennett-Guerrero, Elliott, Berkowitz, Dan E., Birch, Martin, Body, Simon C., Bowdle, T. Andrew, Chambers, Charles E., Chaney, Mark A., Cheng, Alan, Cheng, Davy C.H., Cheung, Albert T., Chikwe, Joanna, Cook, David J., Craner, Ryan C., de Souza, Duncan G., Devaleria, Patrick A., Durieux, Marcel E., Edmonds, Harvey L., Jr., Ender, Joerg Karl, Engelman, Daniel T., Enriquez, Liza J., Feinman, Jared W., Fitzgerald, David, Flier, Suzanne, Fox, Amanda A., Fox, Jonathan F., Freed, Julie K., Freudzon, Leon, Fuster, Valentin, Gelzinis, Theresa A., Ghadimi, Kamrouz, Gordon, Emily K., Groban, Leanne, Grocott, Hilary P., Groom, Robert C., Gutsche, Jacob T., Hensley, Nadia, Hibbert, Benjamin, Higgins, Thomas L., Hinchey, Joseph, Hogue, Charles W., Horrow, Jay, Housmans, Philippe R., Kahn, Ronald A., Kaplan, Joel A., Karkouti, Keyvan, Koch, Colleen G., Kozak, Mark, Lester, Laeben, Levy, Jerrold H., Levy, Warren J., Locke, Adair Q., London, Martin J., Lupei, Monica I., Madani, Michael M., Maus, Timothy, Mitter, Nanhi, Mittnacht, Alexander J.C., Mora-Mangano, Christina T., Morris, Benjamin N., Mounsey, J. Paul, Murkin, John M., Murray, Andrew W., Narula, Jagat, Nathan, Howard J., Nguyen, Liem, Nussmeier, Nancy A., Nuttall, Gregory A., Nyhan, Daniel, O’Brien, Edward R., Oliver, William C., Jr., Pagel, Paul S., Pantin, Enrique J., Patel, Prakash A., Puskas, John D., Quinlan, Joseph J., Ramakrishna, Harish, Ramsay, James G., Rehfeldt, Kent H., Reich, David L., Rhee, Amanda J., Roth, David M., Royster, Roger L., Rozner, Marc A., Salgo, Ivan, Sander, Michael, Savino, Joseph S., Schindler, John, Sengupta, Partho P., Shah, Ashish, Shanewise, Jack S., Sharma, Sonal, Sherman, Benjamin, Shernan, Stanton K., Shore-Lesserson, Linda, Simard, Trevor, Slaughter, Thomas F., Smith, Mark M., Spiess, Bruce D., Stafford-Smith, Mark, Stone, Marc E., Wahr, Joyce A., Wall, Michael, Weiner, Menachem M., Weinkauf, Julia, Weiss, Stuart J., Weitzel, Nathaen, Whitlock, Richard, Zaidan, James R., and Zakhary, Waseem Zakaria Aziz

Published
2020
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125. Neuron‐specific caveolin‐1 overexpression improves motor function and preserves memory in mice subjected to brain trauma

Author

Egawa, Junji, primary, Schilling, Jan M., additional, Cui, Weihua, additional, Posadas, Edmund, additional, Sawada, Atsushi, additional, Alas, Basheer, additional, Zemljic‐Harpf, Alice E., additional, Fannon‐Pavlich, McKenzie J., additional, Mandyam, Chitra D., additional, Roth, David M., additional, Patel, Hemal H., additional, Patel, Piyush M., additional, and Head, Brian P., additional

Published
2017
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132. Cardiac‐specific overexpression of caveolin‐3 preserves t‐tubular ICa during heart failure in mice.

Author

Kong, Cherrie H. T., Bryant, Simon M., Watson, Judy J., Roth, David M., Patel, Hemal H., Cannell, Mark B., James, Andrew F., and Orchard, Clive H.

Subjects
HEART failure, CARDIAC hypertrophy, HEART dilatation, MICE, HYPERTROPHY
Abstract

New Findings: What is the central question of this study?What is the cellular basis of the protection conferred on the heart by overexpression of caveolin‐3 (Cav‐3 OE) against many of the features of heart failure normally observed in vivo?What is the main finding and its importance?Cav‐3 overexpression has little effect in normal ventricular myocytes but reduces cellular hypertrophy and preserves t‐tubular ICa, but not local t‐tubular Ca2+ release, in heart failure induced by pressure overload in mice. Thus Cav‐3 overexpression provides specific but limited protection following induction of heart failure, although other factors disrupt Ca2+ release. Caveolin‐3 (Cav‐3) is an 18 kDa protein that has been implicated in t‐tubule formation and function in cardiac ventricular myocytes. During cardiac hypertrophy and failure, Cav‐3 expression decreases, t‐tubule structure is disrupted and excitation–contraction coupling (ECC) is impaired. Previous work has suggested that Cav‐3 overexpression (OE) is cardio‐protective, but the effect of Cav‐3 OE on these cellular changes is unknown. We therefore investigated whether Cav‐3 OE in mice is protective against the cellular effects of pressure overload induced by 8 weeks' transverse aortic constriction (TAC). Cav‐3 OE mice developed cardiac dilatation, decreased stroke volume and ejection fraction, and hypertrophy and pulmonary congestion in response to TAC. These changes were accompanied by cellular hypertrophy, a decrease in t‐tubule regularity and density, and impaired local Ca2+ release at the t‐tubules. However, the extent of cardiac and cellular hypertrophy was reduced in Cav‐3 OE compared to WT mice, and t‐tubular Ca2+ current (ICa) density was maintained. These data suggest that Cav‐3 OE helps prevent hypertrophy and loss of t‐tubular ICa following TAC, but that other factors disrupt local Ca2+ release. [ABSTRACT FROM AUTHOR]

Published
2019
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133. Caveolin-1 regulation of disrupted-in-schizophrenia-1 as a potential therapeutic target for schizophrenia.

Author

Kassan, Adam, Kassan, Adam, Egawa, Junji, Zhang, Zheng, Almenar-Queralt, Angels, Nguyen, Quynh My, Lajevardi, Yasaman, Kim, Kaitlyn, Posadas, Edmund, Jeste, Dilip V, Roth, David M, Patel, Piyush M, Patel, Hemal H, Head, Brian P, Kassan, Adam, Kassan, Adam, Egawa, Junji, Zhang, Zheng, Almenar-Queralt, Angels, Nguyen, Quynh My, Lajevardi, Yasaman, Kim, Kaitlyn, Posadas, Edmund, Jeste, Dilip V, Roth, David M, Patel, Piyush M, Patel, Hemal H, and Head, Brian P

Abstract

Schizophrenia is a debilitating psychiatric disorder manifested in early adulthood. Disrupted-in-schizophrenia-1 (DISC1) is a susceptible gene for schizophrenia (Hodgkinson et al. 2004; Millar et al. 2000; St Clair et al. 1990) implicated in neuronal development, brain maturation, and neuroplasticity (Brandon and Sawa 2011; Chubb et al. 2008). Therefore, DISC1 is a promising candidate gene for schizophrenia, but the molecular mechanisms underlying its role in the pathogenesis of the disease are still poorly understood. Interestingly, caveolin-1 (Cav-1), a cholesterol binding and scaffolding protein, regulates neuronal signal transduction and promotes neuroplasticity. In this study we examined the role of Cav-1 in mediating DISC1 expression in neurons in vitro and the hippocampus in vivo. Overexpressing Cav-1 specifically in neurons using a neuron-specific synapsin promoter (SynCav1) increased expression of DISC1 and proteins involved in synaptic plasticity (PSD95, synaptobrevin, synaptophysin, neurexin, and syntaxin 1). Similarly, SynCav1-transfected differentiated human neurons derived from induced pluripotent stem cells (hiPSCs) exhibited increased expression of DISC1 and markers of synaptic plasticity. Conversely, hippocampi from Cav-1 knockout (KO) exhibited decreased expression of DISC1 and proteins involved in synaptic plasticity. Finally, SynCav1 delivery to the hippocampus of Cav-1 KO mice and Cav-1 KO neurons in culture restored expression of DISC1 and markers of synaptic plasticity. Furthermore, we found that Cav-1 coimmunoprecipitated with DISC1 in brain tissue. These findings suggest an important role by which neuron-targeted Cav-1 regulates DISC1 neurobiology with implications for synaptic plasticity. Therefore, SynCav1 might be a potential therapeutic target for restoring neuronal function in schizophrenia.New & noteworthyThe present study is the first to demonstrate that caveolin-1 can regulate DISC1 expression in neuronal models. Furthermore, the

Published
2017

134. Neuron-Targeted Caveolin-1 Improves Molecular Signaling, Plasticity, and Behavior Dependent on the Hippocampus in Adult and Aged Mice.

Author

Mandyam, Chitra D, Mandyam, Chitra D, Schilling, Jan M, Cui, Weihua, Egawa, Junji, Niesman, Ingrid R, Kellerhals, Sarah E, Staples, Miranda C, Busija, Anna R, Risbrough, Victoria B, Posadas, Edmund, Grogman, Grace C, Chang, Jamie W, Roth, David M, Patel, Piyush M, Patel, Hemal H, Head, Brian P, Mandyam, Chitra D, Mandyam, Chitra D, Schilling, Jan M, Cui, Weihua, Egawa, Junji, Niesman, Ingrid R, Kellerhals, Sarah E, Staples, Miranda C, Busija, Anna R, Risbrough, Victoria B, Posadas, Edmund, Grogman, Grace C, Chang, Jamie W, Roth, David M, Patel, Piyush M, Patel, Hemal H, and Head, Brian P

Abstract

BackgroundStudies in vitro demonstrate that neuronal membrane/lipid rafts (MLRs) establish cell polarity by clustering progrowth receptors and tethering cytoskeletal machinery necessary for neuronal sprouting. However, the effect of MLR and MLR-associated proteins on neuronal aging is unknown.MethodsHere, we assessed the impact of neuron-targeted overexpression of an MLR scaffold protein, caveolin-1 (Cav-1) (via a synapsin promoter, SynCav1), in the hippocampus in vivo in adult (6-month-old) and aged (20-month-old) mice on biochemical, morphologic, and behavioral changes.ResultsSynCav1 resulted in increased expression of Cav-1, MLRs, and MLR-localization of Cav-1 and tropomyosin-related kinase B receptor independent of age and time post gene transfer. Cav-1 overexpression in adult mice enhanced dendritic arborization within the apical dendrites of hippocampal cornu ammonis 1 and granule cell neurons, effects that were also observed in aged mice, albeit to a lesser extent, indicating preserved impact of Cav-1 on structural plasticity of hippocampal neurons with age. Cav-1 overexpression enhanced contextual fear memory in adult and aged mice demonstrating improved hippocampal function.ConclusionsNeuron-targeted overexpression of Cav-1 in the adult and aged hippocampus enhances functional MLRs with corresponding roles in cell signaling and protein trafficking. The resultant structural alterations in hippocampal neurons in vivo are associated with improvements in hippocampal-dependent learning and memory. Our findings suggest Cav-1 as a novel therapeutic strategy in disorders involving impaired hippocampal function.

Published
2017

135. Colaboradores

Author

Akhtar, Shamsuddin, Armour, Sarah, Auger, William R., Augoustides, John G.T., Badescu, Gina C., Bailey, James M., Bainbridge, Daniel, Banks, Dalia A., Bansal, Manish, Barash, Paul G., Baum, Victor C., Bennett-Guerrero, Elliott, Berkowitz, Dan E., Birch, Martin, Body, Simon C., Bowdle, T. Andrew, Chambers, Charles E., Chaney, Mark A., Cheng, Alan, Cheng, Davy C.H., Cheung, Albert T., Chikwe, Joanna, Cook, David J., Craner, Ryan C., de Souza, Duncan G., Devaleria, Patrick A., Durieux, Marcel E., Edmonds, Harvey L., Jr., Ender, Joerg Karl, Engelman, Daniel T., Enriquez, Liza J., Feinman, Jared W., Fitzgerald, David, Flier, Suzanne, Fox, Amanda A., Fox, Jonathan F., Freed, Julie K., Freudzon, Leon, Fuster, Valentin, Gelzinis, Theresa A., Ghadimi, Kamrouz, Gordon, Emily K., Groban, Leanne, Grocott, Hilary P., Groom, Robert C., Gutsche, Jacob T., Hensley, Nadia, Hibbert, Benjamin, Higgins, Thomas L., Hinchey, Joseph, Hogue, Charles W., Horrow, Jay, Housmans, Philippe R., Kahn, Ronald A., Kaplan, Joel A., Karkouti, Keyvan, Koch, Colleen G., Kozak, Mark, Lester, Laeben, Levy, Jerrold H., Levy, Warren J., Locke, Adair Q., London, Martin J., Lupei, Monica I., Madani, Michael M., Maus, Timothy, Mitter, Nanhi, Mittnacht, Alexander J.C., Mora-Mangano, Christina T., Morris, Benjamin N., Mounsey, J. Paul, Murkin, John M., Murray, Andrew W., Narula, Jagat, Nathan, Howard J., Nguyen, Liem, Nussmeier, Nancy A., Nuttall, Gregory A., Nyhan, Daniel, O’Brien, Edward R., Oliver, William C., Jr., Pagel, Paul S., Pantin, Enrique J., Patel, Prakash A., Puskas, John D., Quinlan, Joseph J., Ramakrishna, Harish, Ramsay, James G., Rehfeldt, Kent H., Reich, David L., Rhee, Amanda J., Roth, David M., Royster, Roger L., Rozner, Marc A., Salgo, Ivan, Sander, Michael, Savino, Joseph S., Schindler, John, Sengupta, Partho P., Shah, Ashish, Shanewise, Jack S., Sharma, Sonal, Sherman, Benjamin, Shernan, Stanton K., Shore-Lesserson, Linda, Simard, Trevor, Slaughter, Thomas F., Smith, Mark M., Spiess, Bruce D., Stafford-Smith, Mark, Stone, Marc E., Wahr, Joyce A., Wall, Michael, Weiner, Menachem M., Weinkauf, Julia, Weiss, Stuart J., Weitzel, Nathaen, Whitlock, Richard, Zaidan, James R., and Zakhary, Waseem Zakaria Aziz

Published
2019
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136. Caveolin-1 regulation of disrupted-in-schizophrenia-1 as a potential therapeutic target for schizophrenia

Author

Kassan, Adam, primary, Egawa, Junji, additional, Zhang, Zheng, additional, Almenar-Queralt, Angels, additional, Nguyen, Quynh My, additional, Lajevardi, Yasaman, additional, Kim, Kaitlyn, additional, Posadas, Edmund, additional, Jeste, Dilip V., additional, Roth, David M., additional, Patel, Piyush M., additional, Patel, Hemal H., additional, and Head, Brian P., additional

Published
2017
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137. Neuron-Targeted Caveolin-1 Improves Molecular Signaling, Plasticity, and Behavior Dependent on the Hippocampus in Adult and Aged Mice

Author

Mandyam, Chitra D., primary, Schilling, Jan M., additional, Cui, Weihua, additional, Egawa, Junji, additional, Niesman, Ingrid R., additional, Kellerhals, Sarah E., additional, Staples, Miranda C., additional, Busija, Anna R., additional, Risbrough, Victoria B., additional, Posadas, Edmund, additional, Grogman, Grace C., additional, Chang, Jamie W., additional, Roth, David M., additional, Patel, Piyush M., additional, Patel, Hemal H., additional, and Head, Brian P., additional

Published
2017
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138. Caveolin-1 regulation of DISC1 as a potential therapeutic target for schizophrenia

Author

Kassan, Adam, Kassan, Adam, Egawa, Junji, Zhang, Zheng, Lajevardi, Yasaman, Kim, Kaitlyn, Nguyen, Quynh My, Posadas, Edmund S, Sawada, Atsushi, Jeste, Dilip V, Roth, David M, Patel, Piyush M, Patel, Hemal H, Head, Brian P, Kassan, Adam, Kassan, Adam, Egawa, Junji, Zhang, Zheng, Lajevardi, Yasaman, Kim, Kaitlyn, Nguyen, Quynh My, Posadas, Edmund S, Sawada, Atsushi, Jeste, Dilip V, Roth, David M, Patel, Piyush M, Patel, Hemal H, and Head, Brian P

Published
2016

139. Electrophysiology and metabolism of caveolin-3-overexpressing mice.

Author

Schilling, Jan M, Schilling, Jan M, Horikawa, Yousuke T, Zemljic-Harpf, Alice E, Vincent, Kevin P, Tyan, Leonid, Yu, Judith K, McCulloch, Andrew D, Balijepalli, Ravi C, Patel, Hemal H, Roth, David M, Schilling, Jan M, Schilling, Jan M, Horikawa, Yousuke T, Zemljic-Harpf, Alice E, Vincent, Kevin P, Tyan, Leonid, Yu, Judith K, McCulloch, Andrew D, Balijepalli, Ravi C, Patel, Hemal H, and Roth, David M

Abstract

Caveolin-3 (Cav-3) plays a critical role in organizing signaling molecules and ion channels involved in cardiac conduction and metabolism. Mutations in Cav-3 are implicated in cardiac conduction abnormalities and myopathies. Additionally, cardiac-specific overexpression of Cav-3 (Cav-3 OE) is protective against ischemic and hypertensive injury, suggesting a potential role for Cav-3 in basal cardiac electrophysiology and metabolism involved in stress adaptation. We hypothesized that overexpression of Cav-3 may alter baseline cardiac conduction and metabolism. We examined: (1) ECG telemetry recordings at baseline and during pharmacological interventions, (2) ion channels involved in cardiac conduction with immunoblotting and computational modeling, and (3) baseline metabolism in Cav-3 OE and transgene-negative littermate control mice. Cav-3 OE mice had decreased heart rates, prolonged PR intervals, and shortened QTc intervals with no difference in activity compared to control mice. Dobutamine or propranolol did not cause significant changes between experimental groups in maximal (dobutamine) or minimal (propranolol) heart rate. Cav-3 OE mice had an overall lower chronotropic response to atropine. The expression of Kv1.4 and Kv4.3 channels, Nav1.5 channels, and connexin 43 were increased in Cav-3 OE mice. A computational model integrating the immunoblotting results indicated shortened action potential duration in Cav-3 OE mice linking the change in channel expression to the observed electrophysiology phenotype. Metabolic profiling showed no gross differences in VO2, VCO2, respiratory exchange ratio, heat generation, and feeding or drinking. In conclusion, Cav-3 OE mice have changes in ECG intervals, heart rates, and cardiac ion channel expression. These findings give novel mechanistic insights into previously reported Cav-3 dependent cardioprotection.

Published
2016

146. Caveolin‐1 regulation of DISC1 as a potential therapeutic target for schizophrenia

Author

Kassan, Adam, primary, Egawa, Junji, additional, Zhang, Zheng, additional, Lajevardi, Yasaman, additional, Kim, Kaitlyn, additional, Nguyen, Quynh My, additional, Posadas, Edmund S., additional, Sawada, Atsushi, additional, Jeste, Dilip V., additional, Roth, David M., additional, Patel, Piyush M., additional, Patel, Hemal H., additional, and Head, Brian P., additional

Published
2016
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149. Electrophysiology and metabolism of caveolin-3-overexpressing mice

Author

Schilling, Jan M., primary, Horikawa, Yousuke T., additional, Zemljic-Harpf, Alice E., additional, Vincent, Kevin P., additional, Tyan, Leonid, additional, Yu, Judith K., additional, McCulloch, Andrew D., additional, Balijepalli, Ravi C., additional, Patel, Hemal H., additional, and Roth, David M., additional

Published
2016
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