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3. Multiomics analyses reveal dynamic bioenergetic pathways and functional remodeling of the heart during intermittent fasting

Author

Arumugam, Thiruma V, primary, Alli-Shaik, Asfa, primary, Liehn, Elisa A, additional, Selvaraji, Sharmelee, additional, Poh, Luting, additional, Rajeev, Vismitha, additional, Cho, Yoonsuk, additional, Cho, Yongeun, additional, Kim, Jongho, additional, Kim, Joonki, additional, Swa, Hannah LF, additional, Hao, David Tan Zhi, additional, Rattanasopa, Chutima, additional, Fann, David Yang-Wei, additional, Mayan, David Castano, additional, Ng, Gavin Yong-Quan, additional, Baik, Sang-Ha, additional, Mallilankaraman, Karthik, additional, Gelderblom, Mathias, additional, Drummond, Grant R, additional, Sobey, Christopher G, additional, Kennedy, Brian K, additional, Singaraja, Roshni R, additional, Mattson, Mark P, additional, Jo, Dong-Gyu, additional, and Gunaratne, Jayantha, additional

Published
2023
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4. Author Response: Multiomics analyses reveal dynamic bioenergetic pathways and functional remodeling of the heart during intermittent fasting

Author

Arumugam, Thiruma, primary, Alli-Shaik, Asfa, additional, Liehn, Elisa A, additional, Selvaraji, Sharmelee, additional, Poh, Luting, additional, Rajeev, Vismitha, additional, Cho, Yoonsuk, additional, Cho, Yongeun, additional, Kim, Jongho, additional, Kim, Joonki, additional, Swa, Hannah LF, additional, Hao, David Tan Zhi, additional, Rattanasopa, Chutima, additional, Fann, David Yang-Wei, additional, Mayan, David Castano, additional, Ng, Gavin Yong-Quan, additional, Baik, Sang-Ha, additional, Mallilankaraman, Karthik, additional, Gelderblom, Mathias, additional, Drummond, Grant R, additional, Sobey, Christopher G, additional, Kennedy, Brian K, additional, Singaraja, Roshni R, additional, Mattson, Mark, additional, Jo, Dong-Gyu, additional, and Gunaratne, Jayantha, additional

Published
2023
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5. FURIN Inhibition Reduces Vascular Remodeling and Atherosclerotic Lesion Progression in Mice

Author

Yakala, Gopala K., Cabrera-Fuentes, Hector A., Crespo-Avilan, Gustavo E., Rattanasopa, Chutima, Burlacu, Alexandrina, George, Benjamin L., Anand, Kaviya, Mayan, David Castaño, Corlianò, Maria, Hernández-Reséndiz, Sauri, Wu, Zihao, Schwerk, Anne M.K., Tan, Amberlyn L.J., Trigueros-Motos, Laia, Chèvre, Raphael, Chua, Tricia, Kleemann, Robert, Liehn, Elisa A., Hausenloy, Derek J., Ghosh, Sujoy, and Singaraja, Roshni R.

Published
2019
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6. Semaphorin3F reduces vascular endothelial and smooth muscle cell PI3K activation and decreases neointimal plaque formation

Author

Rattanasopa, Chutima, primary, Castano-Mayan, David, additional, Su, Chengxun, additional, Farrugia, Aaron J., additional, Corlianò, Maria, additional, Nilcham, Pakhwan, additional, Pang, Crystal, additional, Hota, Monalisa, additional, Mei, Koh Ser, additional, Lee, Wendy, additional, Cibi, Dasan Mary, additional, Aiba, Atsu, additional, Singh, Manvendra K., additional, Wong, Siew Cheng, additional, Rotzschke, Olaf, additional, Bershadsky, Alexander, additional, Hou, Han Wei, additional, Liehn, Elisa A., additional, Ghosh, Sujoy, additional, and Singaraja, Roshni R., additional

Published
2022
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7. Caffeine prevents restenosis and inhibits vascular smooth muscle cell proliferation through the induction of autophagy

Author

Tripathi, Madhulika, primary, Singh, Brijesh Kumar, additional, Liehn, Elisa A., additional, Lim, Sheau Yng, additional, Tikno, Keziah, additional, Castano-Mayan, David, additional, Rattanasopa, Chutima, additional, Nilcham, Pakhwan, additional, Abdul Ghani, Siti Aishah Binte, additional, Wu, Zihao, additional, Azhar, Syaza Hazwany, additional, Zhou, Jin, additional, Hernández-Resèndiz, Sauri, additional, Crespo-Avilan, Gustavo E., additional, Sinha, Rohit Anthony, additional, Farah, Benjamin Livingston, additional, Moe, Kyaw Thu, additional, De Silva, Deidre Anne, additional, Angeli, Veronique, additional, Singh, Manvendra K., additional, Singaraja, Roshni R., additional, Hausenloy, Derek J., additional, and Yen, Paul Michael, additional

Published
2022
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12. Abstract 11736: Semaphorin 3F Inhibits Transendothelial Monocyte Migration and Protects Against Atherosclerosis

Author

Rattanasopa, Chutima, Pang, Crystal Kok Yan, Liehn, Elisa, Castano, David, Singaraja, Roshni R, and Ghosh, Sujoy

Abstract

Objectives:Accumulating evidence suggests a role of semaphorin 3F (Sema3F) in heart development, immune responses and tumor growth inhibition. Genetic analyses suggest that semaphorin signaling associates with coronary artery disease, but the roles of specific semaphorin subtypes remain unexplored. Here, we aim to elucidate a potentially novel role for Sema3F in atherosclerosis.Methods and Results:Atherosclerosis was induced via partial ligation of the common carotid in 12 week old Sema3F-/-and litter-mate control mice fed with the Western type diet (WTD) for 5 weeks. Deletion of Sema3F significantly increased atherosclerotic lesion area in the Sema3F-/-mice (48% increase, p=0.008). Conversely, exogenous Sema3F protein was injected (100ng/kg, ip, 3X weekly) into 12 week old WTD-fed Ldlr-/-mice that had undergone carotid endothelial cell denudation via wire injury for 3 weeks to establish restenosis-driven plaque formation. Sema3F overexpression significantly reduced plaque formation in this model (56% decrease, p=0.0006). Macrophage numbers were significantly lower in plaques from the wire-injured mice overexpressing Sema3F (66% lower, p=0.001), with no changes in smooth muscle cell number. Since macrophage numbers were decreased in the plaques of the mice over-expressing Sema3F, we tested the impact of endothelial Sema3F on monocyte adhesion/migration utilizing a micro-engineered perfusable 3D vasculature model. Aortic endothelial cells from Sema3F-/-and WT mice were seeded onto the flow chamber and allowed to form a confluent monolayer, followed by perfusion with THP-1 monocytes. Significantly greater adhesion/migration of monocytes to endothelial cells from Sema3F-/-were found (50% increase, p=0.01), suggesting that Sema3F mediates its protective effects on atherosclerosis in part through inhibiting monocyte/macrophage infiltration.Conclusions:These data show that Sema3F plays a significant and potentially causal role in atherosclerosis/restenosis, and establish a novel role for semaphorins in large vessel disease. Approaches to increase Sema3F levels may represent a novel therapeutic avenue for the prevention and treatment of atherosclerosis.

Published
2019
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13. Estrogen but not testosterone preserves myofilament function from doxorubicin-induced cardiotoxicity by reducing oxidative modifications.

Author

Rattanasopa C, Kirk JA, Bupha-Intr T, Papadaki M, de Tombe PP, and Wattanapermpool J

Subjects
Animals, Calcium metabolism, Cardiotoxicity, Estrogens metabolism, Female, Male, Myocardial Contraction, Myofibrils drug effects, Myofibrils metabolism, Myofibrils physiology, Oxidative Stress, Papillary Muscles drug effects, Papillary Muscles physiology, Phosphorylation, Protein Processing, Post-Translational, Rats, Rats, Sprague-Dawley, Sex Factors, Testosterone metabolism, Troponin I metabolism, Antioxidants pharmacology, Doxorubicin toxicity, Estrogens pharmacology, Papillary Muscles metabolism, Testosterone pharmacology
Abstract

Here, we aimed to explore sex differences and the impact of sex hormones on cardiac contractile properties in doxorubicin (DOX)-induced cardiotoxicity. Male and female Sprague-Dawley rats were subjected to sham surgery or gonadectomy and then treated or untreated with DOX (2 mg/kg) every other week for 10 wk. Estrogen preserved maximum active tension (T max ) with DOX exposure, whereas progesterone and testosterone did not. The effects of sex hormones and DOX correlated with both altered myosin heavy chain isoform expression and myofilament protein oxidation, suggesting both as possible mechanisms. However, acute treatment with oxidative stress (H 2 O 2 ) or a reducing agent (DTT) indicated that the effects on T max were mediated by reversible myofilament oxidative modifications and not only changes in myosin heavy chain isoforms. There were also sex differences in the DOX impact on myofilament Ca 2+ sensitivity. DOX increased Ca 2+ sensitivity in male rats only in the absence of testosterone and in female rats only in the presence of estrogen. Conversely, DOX decreased Ca 2+ sensitivity in female rats in the absence of estrogen. In most instances, this mechanism was through altered phosphorylation of troponin I at Ser 23 /Ser 24 . However, there was an additional DOX-induced, estrogen-dependent, irreversible (by DTT) mechanism that altered Ca 2+ sensitivity. Our data demonstrate sex differences in cardiac contractile responses to chronic DOX treatment. We conclude that estrogen protects against chronic DOX treatment in the heart, preserving myofilament function. NEW & NOTEWORTHY We identified sex differences in cardiotoxic effects of chronic doxorubicin (DOX) exposure on myofilament function. Estrogen, but not testosterone, decreases DOX-induced oxidative modifications on myofilaments to preserve maximum active tension. In rats, DOX exposure increased Ca 2+ sensitivity in the presence of estrogen but decreased Ca 2+ sensitivity in the absence of estrogen. In male rats, the DOX-induced shift in Ca 2+ sensitivity involved troponin I phosphorylation; in female rats, this was through an estrogen-dependent mechanism.

Published
2019
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