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26 results on '"Tham, Yow Keat"'

1. Estrogen receptor alpha deficiency in cardiomyocytes reprograms the heart-derived extracellular vesicle proteome and induces obesity in female mice

Author

Tham, Yow Keat, Bernardo, Bianca C., Claridge, Bethany, Yildiz, Gunes S., Woon, Liesel Min-Linn, Bond, Simon, Fang, Haoyun, Ooi, Jenny Y. Y., Matsumoto, Aya, Luo, Jieting, Tai, Celeste M. K., Harmawan, Claudia A., Kiriazis, Helen, Donner, Daniel G., Mellett, Natalie A., Abel, E. Dale, Khan, Sohaib A., De Souza, David P., Doomun, Sheik Nadeem Elahee, Liu, Kevin, Xiang, Ruidong, Singh, Manika, Inouye, Michael, Meikle, Peter J., Weeks, Kate L., Drew, Brian G., Greening, David W., and McMullen, Julie R.

Published
2023
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3. Estrogen receptor α deficiency in cardiac myocytes reprograms heart-derived extracellular vesicle proteome and induces obesity in female mice

Author

Tham, Yow Keat, primary, Bernardo, Bianca, additional, Claridge, Bethany, additional, Woon, Liesel, additional, Yildiz, Gunes, additional, Ooi, Jenny, additional, Matsumoto, Aya, additional, Luo, Jieting, additional, Tai, Celeste, additional, Harmawan, Claudia, additional, Kiriazis, Helen, additional, Donner, Daniel, additional, Mellett, Natalie, additional, Abel, Dale, additional, Khan, Sohaib, additional, Meikle, Peter, additional, Weeks, Kate, additional, Greening, David, additional, and McMullen, Julie, additional

Published
2022
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4. CD14 inhibition mitigates left ventricular damage and dysfunction following myocardial infarction

Author

Brown, Aascha, primary, Kiriazis, Helen, additional, Tai, Tsin Yee, additional, Parslow, Adam, additional, Johnson, Chad, additional, Jansen, Stephanie, additional, Tham, Yow Keat, additional, Cohen, Camilla, additional, Vais, Angela, additional, Krippner, Guy, additional, Wang, Bing, additional, Kaye, David, additional, and Donner, Daniel, additional

Published
2022
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8. FoxO1 is required for physiological cardiac hypertrophy induced by exercise but not by constitutively active PI3K

Author

Weeks, Kate L., primary, Tham, Yow Keat, additional, Yildiz, Suzan G., additional, Alexander, Yonali, additional, Donner, Daniel G., additional, Kiriazis, Helen, additional, Harmawan, Claudia A., additional, Hsu, Amy, additional, Bernardo, Bianca C., additional, Matsumoto, Aya, additional, DePinho, Ronald A., additional, Abel, E. Dale, additional, Woodcock, Elizabeth A., additional, and McMullen, Julie R., additional

Published
2021
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9. Novel lipid species for detecting and predicting atrial fibrillation in patients with type 2 diabetes

Author

Admin, Ada, primary, Tham, Yow Keat, primary, Jayawardana, Kaushala S., primary, Alshehry, Zahir H., primary, Giles, Corey, primary, Huynh, Kevin, primary, Smith, Adam Alexander T., primary, Ooi, Jenny Y. Y., primary, Zoungas, Sophia, primary, Hillis, Graham S., primary, Chalmers, John, primary, Meikle, Peter J., primary, and McMullen, Julie R., primary

Published
2020
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10. Novel Lipid Species for Detecting and Predicting Atrial Fibrillation in Patients With Type 2 Diabetes

Author

Tham, Yow Keat, primary, Jayawardana, Kaushala S., additional, Alshehry, Zahir H., additional, Giles, Corey, additional, Huynh, Kevin, additional, Smith, Adam Alexander T., additional, Ooi, Jenny Y.Y., additional, Zoungas, Sophia, additional, Hillis, Graham S., additional, Chalmers, John, additional, Meikle, Peter J., additional, and McMullen, Julie R., additional

Published
2020
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12. Novel Lipid Species for Detecting and Predicting Atrial Fibrillation in Patients With Type 2 Diabetes.

Author

Tham, Yow Keat, Jayawardana, Kaushala S., Alshehry, Zahir H., Giles, Corey, Huynh, Kevin, Smith, Adam Alexander T., Ooi, Jenny Y.Y., Zoungas, Sophia, Hillis, Graham S., Chalmers, John, Meikle, Peter J., and McMullen, Julie R.

Subjects
*ATRIAL fibrillation, *FORECASTING, *TYPE 2 diabetes, *BLOOD lipids, *LIPIDS, *ATRIAL fibrillation diagnosis, *RESEARCH, *ANIMAL experimentation, *RESEARCH methodology, *MEDICAL cooperation, *EVALUATION research, *RISK assessment, *COMPARATIVE studies, *MICE, *DISEASE complications
Abstract

The incidence of atrial fibrillation (AF) is higher in patients with diabetes. The goal of this study was to assess if the addition of plasma lipids to traditional risk factors could improve the ability to detect and predict future AF in patients with type 2 diabetes. Logistic regression models were used to identify lipids associated with AF or future AF from plasma lipids (n = 316) measured from participants in the ADVANCE trial (n = 3,772). To gain mechanistic insight, follow-up lipid analysis was undertaken in a mouse model that has an insulin-resistant heart and is susceptible to AF. Sphingolipids, cholesteryl esters, and phospholipids were associated with AF prevalence, whereas two monosialodihexosylganglioside (GM3) ganglioside species were associated with future AF. For AF detection and prediction, addition of six and three lipids, respectively, to a base model (n = 12 conventional risk factors) increased the C-statistics (detection: from 0.661 to 0.725; prediction: from 0.674 to 0.715) and categorical net reclassification indices. The GM3(d18:1/24:1) level was lower in patients in whom AF developed, improved the C-statistic for the prediction of future AF, and was lower in the plasma of the mouse model susceptible to AF. This study demonstrates that plasma lipids have the potential to improve the detection and prediction of AF in patients with diabetes. [ABSTRACT FROM AUTHOR]

Published
2021
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14. Distinct lipidomic profiles in models of physiological and pathological cardiac remodeling, and potential therapeutic strategies

Author

Tham, Yow Keat, primary, Huynh, Kevin, additional, Mellett, Natalie A., additional, Henstridge, Darren C., additional, Kiriazis, Helen, additional, Ooi, Jenny Y.Y., additional, Matsumoto, Aya, additional, Patterson, Natalie L., additional, Sadoshima, Junichi, additional, Meikle, Peter J., additional, and McMullen, Julie R., additional

Published
2018
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15. Gene delivery of medium chain acyl-coenzyme A dehydrogenase induces physiological cardiac hypertrophy and protects against pathological remodelling

Author

Bernardo, Bianca C., primary, Weeks, Kate L., additional, Pongsukwechkul, Thawin, additional, Gao, Xiaoming, additional, Kiriazis, Helen, additional, Cemerlang, Nelly, additional, Boey, Esther J.H., additional, Tham, Yow Keat, additional, Johnson, Chad J., additional, Qian, Hongwei, additional, Du, Xiao-Jun, additional, Gregorevic, Paul, additional, and McMullen, Julie R., additional

Published
2018
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17. Sex differences in response to miRNA‐34a therapy in mouse models of cardiac disease: identification of sex‐, disease‐ and treatment‐regulated miRNAs

Author

Bernardo, Bianca C., primary, Ooi, Jenny Y. Y., additional, Matsumoto, Aya, additional, Tham, Yow Keat, additional, Singla, Saloni, additional, Kiriazis, Helen, additional, Patterson, Natalie L., additional, Sadoshima, Junichi, additional, Obad, Susanna, additional, Lin, Ruby C. Y., additional, and McMullen, Julie R., additional

Published
2016
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18. The small-molecule BGP-15 protects against heart failure and atrial fibrillation in mice

Author

Sapra, Geeta, primary, Tham, Yow Keat, additional, Cemerlang, Nelly, additional, Matsumoto, Aya, additional, Kiriazis, Helen, additional, Bernardo, Bianca C., additional, Henstridge, Darren C., additional, Ooi, Jenny Y. Y., additional, Pretorius, Lynette, additional, Boey, Esther J. H., additional, Lim, Lydia, additional, Sadoshima, Junichi, additional, Meikle, Peter J., additional, Mellet, Natalie A., additional, Woodcock, Elizabeth A., additional, Marasco, Silvana, additional, Ueyama, Tomomi, additional, Du, Xiao-Jun, additional, Febbraio, Mark A., additional, and McMullen, Julie R., additional

Published
2014
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19. Therapeutic silencing of miR‐652 restores heart function and attenuates adverse remodeling in a setting of established pathological hypertrophy

Author

Bernardo, Bianca C., primary, Nguyen, Sally S., additional, Winbanks, Catherine E., additional, Gao, Xiao‐Ming, additional, Boey, Esther J. H., additional, Tham, Yow Keat, additional, Kiriazis, Helen, additional, Ooi, Jenny Y. Y., additional, Porrello, Enzo R., additional, Igoor, Sindhu, additional, Thomas, Colleen J., additional, Gregorevic, Paul, additional, Lin, Ruby C. Y., additional, Du, Xiao‐Jun, additional, and McMullen, Julie R., additional

Published
2014
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20. Abstract 50: Therapeutic Silencing of miRNA-652 Restores Cardiac Function and Attenuates Pathological Remodeling in a Mouse Model of Pressure Overload

Author

Bernardo, Bianca C, primary, Nguyen, Sally S, additional, Winbanks, Catherine E, additional, Gao, Xiao-Ming, additional, Boey, Esther J, additional, Tham, Yow Keat, additional, Kiriazis, Helen, additional, Thomas, Colleen J, additional, Lin, Ruby C, additional, Du, Xiao-Jun, additional, and McMullen, Julie R, additional

Published
2014
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21. O166 Inhibition of miRNA-652 Using LNA-antimiRs Improves Cardiac Function in a Mouse Model of Pressure Overload and is Associated with Preserved Angiogenesis and Upregulation of Jagged 1

Author

Bernardo, Bianca C., primary, Nguyen, Sally S., additional, Gao, Xiao-Ming, additional, Boey, Esther J., additional, Tham, Yow Keat, additional, Kiriazis, Helen, additional, Du, Xiao-Jun, additional, Lin, Ruby C., additional, and McMullen, Julie R., additional

Published
2014
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22. Silencing of miR-34a Attenuates Cardiac Dysfunction in a Setting of Moderate, but Not Severe, Hypertrophic Cardiomyopathy

Author

Bernardo, Bianca C., primary, Gao, Xiao-Ming, additional, Tham, Yow Keat, additional, Kiriazis, Helen, additional, Winbanks, Catherine E., additional, Ooi, Jenny Y. Y., additional, Boey, Esther J. H., additional, Obad, Susanna, additional, Kauppinen, Sakari, additional, Gregorevic, Paul, additional, Du, Xiao-Jun, additional, Lin, Ruby C. Y., additional, and McMullen, Julie R., additional

Published
2014
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23. Phosphoinositide 3-Kinase p110α Is a Master Regulator of Exercise-Induced Cardioprotection and PI3K Gene Therapy Rescues Cardiac Dysfunction

Author

Weeks, Kate L., primary, Gao, Xiaoming, additional, Du, Xiao-Jun, additional, Boey, Esther J.H., additional, Matsumoto, Aya, additional, Bernardo, Bianca C., additional, Kiriazis, Helen, additional, Cemerlang, Nelly, additional, Tan, Joon Win, additional, Tham, Yow Keat, additional, Franke, Thomas F., additional, Qian, Hongwei, additional, Bogoyevitch, Marie A., additional, Woodcock, Elizabeth A., additional, Febbraio, Mark A., additional, Gregorevic, Paul, additional, and McMullen, Julie R., additional

Published
2012
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24. Lipids regulated by exercise and phosphoinositide 3-kinase: potential role as biomarkers and therapeutic targets for cardiovascular disease

Author

Belkin, Teleah G, Tham, Yow Keat, and McMullen, Julie R

Abstract

Lipids are organic biomolecules that provide structural support to cells, but are also important for energy storage and signaling. Lipid profiling has emerged as a new technology with the potential of identifying new biomarkers and therapeutic targets. The lipid composition of cardiomyocyte membranes is altered during the process of cardiac remodeling, including exercise-induced heart enlargement (physiological cardiac hypertrophy) and disease-induced pathological remodeling. Phosphoinositide 3-kinase (PI3K) is an essential regulator of exercise-induced physiological hypertrophy and mediator of cardioprotection in cardiac stress settings. In this review, we first briefly summarize the protective role of exercise and PI3K on the heart. Next, we describe the regulation of lipids in the heart and circulation by exercise or transgenic expression of PI3K (increased or decreased), and contrast this to cardiac disease settings. We also describe studies in which exercise or PI3K-regulated lipids have been associated with cardiorespiratory fitness or cardioprotection, and discuss potential clinical applications.

Published
2023
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25. Abstract 50.

Author

Bernardo, Bianca C, Nguyen, Sally S, Winbanks, Catherine E, Gao, Xiao-Ming, Boey, Esther J, Tham, Yow Keat, Kiriazis, Helen, Thomas, Colleen J, Lin, Ruby C, Du, Xiao-Jun, and McMullen, Julie R

Published
2014

26. FoxO1 is required for physiological cardiac hypertrophy induced by exercise but not by constitutively active PI3K.

Author

Weeks KL, Tham YK, Yildiz SG, Alexander Y, Donner DG, Kiriazis H, Harmawan CA, Hsu A, Bernardo BC, Matsumoto A, DePinho RA, Abel ED, Woodcock EA, and McMullen JR

Subjects
Animals, Cardiomegaly genetics, Cardiomegaly pathology, Cardiomegaly physiopathology, Class I Phosphatidylinositol 3-Kinases genetics, Enzyme Activation, Female, Fibrosis, Forkhead Box Protein O1 deficiency, Forkhead Box Protein O1 genetics, Forkhead Box Protein O3 genetics, Forkhead Box Protein O3 metabolism, Gene Expression Regulation, HSP70 Heat-Shock Proteins metabolism, Male, Mice, Knockout, Myocytes, Cardiac pathology, Phenotype, Phosphorylation, Proto-Oncogene Proteins c-akt metabolism, Receptor, IGF Type 1 metabolism, Signal Transduction, Swimming, Mice, Cardiomegaly enzymology, Cardiomegaly, Exercise-Induced, Class I Phosphatidylinositol 3-Kinases metabolism, Forkhead Box Protein O1 metabolism, Myocytes, Cardiac enzymology
Abstract

The insulin-like growth factor 1 receptor (IGF1R) and phosphoinositide 3-kinase p110α (PI3K) are critical regulators of exercise-induced physiological cardiac hypertrophy and provide protection in experimental models of pathological remodeling and heart failure. Forkhead box class O1 (FoxO1) is a transcription factor that regulates cardiomyocyte hypertrophy downstream of IGF1R/PI3K activation in vitro, but its role in physiological hypertrophy in vivo was unknown. We generated cardiomyocyte-specific FoxO1 knockout (cKO) mice and assessed the phenotype under basal conditions and settings of physiological hypertrophy induced by 1 ) swim training or 2 ) cardiac-specific transgenic expression of constitutively active PI3K (caPI3K Tg+ ). Under basal conditions, male and female cKO mice displayed mild interstitial fibrosis compared with control (CON) littermates, but no other signs of cardiac pathology were present. In response to exercise training, female CON mice displayed an increase (∼21%) in heart weight normalized to tibia length vs. untrained mice. Exercise-induced hypertrophy was blunted in cKO mice. Exercise increased cardiac Akt phosphorylation and IGF1R expression but was comparable between genotypes. However, differences in Foxo3a, Hsp70, and autophagy markers were identified in hearts of exercised cKO mice. Deletion of FoxO1 did not reduce cardiac hypertrophy in male or female caPI3K Tg+ mice. Cardiac Akt and FoxO1 protein expressions were significantly reduced in hearts of caPI3K Tg+ mice, which may represent a negative feedback mechanism from chronic caPI3K, and negate any further effect of reducing FoxO1 in the cKO. In summary, FoxO1 contributes to exercise-induced hypertrophy. This has important implications when one is considering FoxO1 as a target for treating the diseased heart. NEW & NOTEWORTHY Regulators of exercise-induced physiological cardiac hypertrophy and protection are considered promising targets for the treatment of heart failure. Unlike pathological hypertrophy, the transcriptional regulation of physiological hypertrophy has remained largely elusive. To our knowledge, this is the first study to show that the transcription factor FoxO1 is a critical mediator of exercise-induced cardiac hypertrophy. Given that exercise-induced hypertrophy is protective, this finding has important implications when one is considering FoxO1 as a target for treating the diseased heart.

Published
2021
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