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  1. Article ; Online: Editorial

    Yuzhen Li / Xianglan Yao / Stewart J. Levine / Sang-Bing Ong

    Frontiers in Molecular Biosciences, Vol

    Organellar dynamics in cell fate

    2022  Volume 9

    Keywords organellar dynamics ; cardiac differentiation ; non-coding RNA ; endoplasmic reticulum ; mitochondria ; cardiomyocyte fate ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2022-08-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Large animal models of cardiac ischemia-reperfusion injury

    Attaur Rahman / Yuhao Li / To-Kiu Chan / Hui Zhao / Yaozu Xiang / Xing Chang / Hao Zhou / Dachun Xu / Sang-Bing Ong

    Zoological Research, Vol 44, Iss 3, Pp 591-

    Where are we now?

    2023  Volume 603

    Abstract: Large animal models of cardiac ischemia-reperfusion are critical for evaluation of the efficacy of cardioprotective interventions prior to clinical translation. Nonetheless, current cardioprotective strategies/interventions formulated in preclinical ... ...

    Abstract Large animal models of cardiac ischemia-reperfusion are critical for evaluation of the efficacy of cardioprotective interventions prior to clinical translation. Nonetheless, current cardioprotective strategies/interventions formulated in preclinical cardiovascular research are often limited to small animal models, which are not transferable or reproducible in large animal models due to different factors such as: (i) complex and varied features of human ischemic cardiac disease (ICD), which are challenging to mimic in animal models, (ii) significant differences in surgical techniques applied, and (iii) differences in cardiovascular anatomy and physiology between small versus large animals. This article highlights the advantages and disadvantages of different large animal models of preclinical cardiac ischemic reperfusion injury (IRI), as well as the different methods used to induce and assess IRI, and the obstacles faced in using large animals for translational research in the settings of cardiac IR.
    Keywords cardiovascular disorder ; ischemic cardiac disease ; ischemic-reperfusion injury ; large animal model ; myocardial infarction ; translational gap ; Zoology ; QL1-991
    Language English
    Publishing date 2023-05-01T00:00:00Z
    Publisher Science Press, PR China
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Editorial

    Martina Iengo / Ester Topa / Alessandra Cuomo / Maria Cristina Luise / Francesco Fiore / Marika Rizza / Mattia Miccio / Elena Di Sarro / Giuseppe Ciaccio / Chiara Di Lorenzo / Valentina Mercurio / Sang-Bing Ong / Serena Zacchigna / Carlo Gabriele Tocchetti

    Frontiers in Molecular Medicine, Vol

    Myocardium regeneration and cardioprotection

    2023  Volume 3

    Keywords myocardium regeneration ; cardioprotection ; stem cells ; cardiomyocytes ; heart failure ; Computer applications to medicine. Medical informatics ; R858-859.7
    Language English
    Publishing date 2023-10-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Detection of viral RNA fragments in human iPSC cardiomyocytes following treatment with extracellular vesicles from SARS-CoV-2 coding sequence overexpressing lung epithelial cells

    Youjeong Kwon / Sarath Babu Nukala / Shubhi Srivastava / Hiroe Miyamoto / Nur Izzah Ismail / Jordan Jousma / Jalees Rehman / Sang-Bing Ong / Won Hee Lee / Sang-Ging Ong

    Stem Cell Research & Therapy, Vol 11, Iss 1, Pp 1-

    2020  Volume 5

    Abstract: Abstract Coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a global pandemic. The prevalence/severity of COVID-19 is higher among patients with cardiovascular risk factors. Despite the ... ...

    Abstract Abstract Coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a global pandemic. The prevalence/severity of COVID-19 is higher among patients with cardiovascular risk factors. Despite the expression of angiotensin-converting enzyme 2 (ACE2), a receptor for SARS-CoV-2 infection, in cardiomyocytes, there has been no conclusive evidence of direct viral infection although the presence of viral genome within COVID-19 patients’ hearts has been reported. Here, we overexpressed SARS-CoV-2 genes in A549 lung epithelial cells. We then isolated extracellular vesicles (EVs) and detected the presence of viral RNA within these EVs. We observed that human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) are receptive to these EVs, and viral genes were detectable in the cardiomyocytes. Accordingly, the uptake of viral RNA-harboring EVs led to an upregulation of inflammation-related genes in hiPSC-CMs. Thus, our findings indicate that SARS-CoV-2 RNA containing EVs represents an indirect route of viral RNA entry into cardiomyocytes.
    Keywords COVID-19 ; Extracellular vesicles ; iPSCs ; Stem cells ; Cardiomyocytes ; Medicine (General) ; R5-920 ; Biochemistry ; QD415-436
    Language English
    Publishing date 2020-11-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Targeting Mitochondrial Fission Using Mdivi-1 in A Clinically Relevant Large Animal Model of Acute Myocardial Infarction

    Sang-Bing Ong / Xiu-Yi Kwek / Khairunnisa Katwadi / Sauri Hernandez-Resendiz / Gustavo E. Crespo-Avilan / Nur Izzah Ismail / Ying-Hsi Lin / En Ping Yap / Song-Yi Lim / K P Myu Mai Ja / Chrishan J.A. Ramachandra / Nicole Tee / Jin Jiat Toh / Winston Shim / Philip Wong / Hector A. Cabrera-Fuentes / Derek J Hausenloy

    International Journal of Molecular Sciences, Vol 20, Iss 16, p

    A Pilot Study

    2019  Volume 3972

    Abstract: Background : New treatments are needed to reduce myocardial infarct size (MI) and prevent heart failure (HF) following acute myocardial infarction (AMI), which are the leading causes of death and disability worldwide. Studies in rodent AMI models showed ... ...

    Abstract Background : New treatments are needed to reduce myocardial infarct size (MI) and prevent heart failure (HF) following acute myocardial infarction (AMI), which are the leading causes of death and disability worldwide. Studies in rodent AMI models showed that genetic and pharmacological inhibition of mitochondrial fission, induced by acute ischemia and reperfusion, reduced MI size. Whether targeting mitochondrial fission at the onset of reperfusion is also cardioprotective in a clinically-relevant large animal AMI model remains to be determined. Methods : Adult pigs (30–40 kg) were subjected to closed-chest 90-min left anterior descending artery ischemia followed by 72 h of reperfusion and were randomized to receive an intracoronary bolus of either mdivi-1 (1.2 mg/kg, a small molecule inhibitor of the mitochondrial fission protein, Drp1) or vehicle control, 10-min prior to reperfusion. The left ventricular (LV) size and function were both assessed by transthoracic echocardiography prior to AMI and after 72 h of reperfusion. MI size and the area-at-risk (AAR) were determined using dual staining with Tetrazolium and Evans blue. Heart samples were collected for histological determination of fibrosis and for electron microscopic analysis of mitochondrial morphology. Results : A total of 14 pigs underwent the treatment protocols (eight control and six mdivi-1). Administration of mdivi-1 immediately prior to the onset of reperfusion did not reduce MI size (MI size as % of AAR: Control 49.2 ± 8.6 vs. mdivi-1 50.5 ± 11.4; p = 0.815) or preserve LV systolic function (LV ejection fraction %: Control 67.5 ± 0.4 vs. mdivi-1 59.6 ± 0.6; p = 0.420), when compared to vehicle control. Similarly, there were no differences in mitochondrial morphology or myocardial fibrosis between mdivi-1 and vehicle control groups. Conclusion : Our pilot study has shown that treatment with mdivi-1 (1.2 mg/kg) at the onset of reperfusion did not reduce MI size or preserve LV function in the clinically-relevant closed-chest pig AMI model. A larger ...
    Keywords mdivi-1 ; mitochondrial morphology ; cardioprotection ; Drp1 ; pig ; ischemia/reperfusion injury ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 630 ; 610
    Language English
    Publishing date 2019-08-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: Loss of PINK1 increases the heart's vulnerability to ischemia-reperfusion injury.

    Hilary K Siddall / Derek M Yellon / Sang-Bing Ong / Uma A Mukherjee / Niall Burke / Andrew R Hall / Plamena R Angelova / Marthe H R Ludtmann / Emma Deas / Sean M Davidson / Mihaela M Mocanu / Derek J Hausenloy

    PLoS ONE, Vol 8, Iss 4, p e

    2013  Volume 62400

    Abstract: Mutations in PTEN inducible kinase-1 (PINK1) induce mitochondrial dysfunction in dopaminergic neurons resulting in an inherited form of Parkinson's disease. Although PINK1 is present in the heart its exact role there is unclear. We hypothesized that ... ...

    Abstract Mutations in PTEN inducible kinase-1 (PINK1) induce mitochondrial dysfunction in dopaminergic neurons resulting in an inherited form of Parkinson's disease. Although PINK1 is present in the heart its exact role there is unclear. We hypothesized that PINK1 protects the heart against acute ischemia reperfusion injury (IRI) by preventing mitochondrial dysfunction.Over-expressing PINK1 in HL-1 cardiac cells reduced cell death following simulated IRI (29.2±5.2% PINK1 versus 49.0±2.4% control; N = 320 cells/group P<0.05), and delayed the onset of mitochondrial permeability transition pore (MPTP) opening (by 1.3 fold; P<0.05). Hearts excised from PINK1+/+, PINK1+/- and PINK1-/- mice were subjected to 35 minutes regional ischemia followed by 30 minutes reperfusion. Interestingly, myocardial infarct size was increased in PINK1-/- hearts compared to PINK1+/+ hearts with an intermediate infarct size in PINK1+/- hearts (25.1±2.0% PINK1+/+, 38.9±3.4% PINK1+/- versus 51.5±4.3% PINK1-/- hearts; N>5 animals/group; P<0.05). Cardiomyocytes isolated from PINK1-/- hearts had a lower resting mitochondrial membrane potential, had inhibited mitochondrial respiration, generated more oxidative stress during simulated IRI, and underwent rigor contracture more rapidly in response to an uncoupler when compared to PINK1+/+ cells suggesting mitochondrial dysfunction in hearts deficient in PINK1.We show that the loss of PINK1 increases the heart's vulnerability to ischemia-reperfusion injury. This may be due, in part, to increased mitochondrial dysfunction. These findings implicate PINK1 as a novel target for cardioprotection.
    Keywords Medicine ; R ; Science ; Q
    Subject code 610
    Language English
    Publishing date 2013-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Correction

    Hilary K. Siddall / Derek M. Yellon / Sang-Bing Ong / Uma A. Mukherjee / Niall Burke / Andrew R. Hall / Plamena R. Angelova / Marthe H. R. Ludtmann / Emma Deas / Sean M. Davidson / Mihaela M. Mocanu / Derek J. Hausenloy

    PLoS ONE, Vol 8, Iss

    Loss of PINK1 Increases the Heart's Vulnerability to Ischemia-Reperfusion Injury

    2013  Volume 6

    Keywords Medicine ; R ; Science ; Q
    Language English
    Publishing date 2013-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Correction

    Hilary K. Siddall / Derek M. Yellon / Sang-Bing Ong / Uma A. Mukherjee / Niall Burke / Andrew R. Hall / Plamena R. Angelova / Marthe H. R. Ludtmann / Emma Deas / Sean M. Davidson / Mihaela M. Mocanu / Derek J. Hausenloy

    PLoS ONE, Vol 8, Iss

    Loss of PINK1 Increases the Heart's Vulnerability to Ischemia-Reperfusion Injury.

    2013  Volume 6

    Keywords Medicine ; R ; Science ; Q
    Language English
    Publishing date 2013-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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