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Schematic illustration of primary rat cardiomyocyte isolation. Healthy male Sprague Dawley rats (n = 14) were anaesthetised and had their hearts excised. The heart was attached to a Langendorff column and different solutions were perfused across various time points to arrest and digest the heart. Ventricles were extracted and bubbled to obtain a pellet of live ventricular cardiomyocytes. Pelleted cardiomyocytes were resuspended in medium 199 and distributed onto sterile culture wells that have been pre-coated with laminin.
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Reductions in cardiac infarct size can be achieved in ischaemic preconditioning, a procedure which subjects the heart to intermittent, non-lethal cycles of ischaemia and reperfusion. Similar cardioprotection can be induced upon preconditioning distal tissues such as the upper limb, and this procedure is called remote ischaemic preconditioning. Nano...
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Objective:
Ginsenoside Rb1 (GRb1) is known to play an effective protection on myocardial infarction, yet its therapeutic mechanism on myocardial ischemia/reperfusion (I/R) injury has remained obscure. Here we sought to investigate the protective mechanism of GRb1 preconditioning on myocardial I/R injury in rats.
Methods and results:
We report he...
Activation of the Akt pathway has been shown to protect the heart from ischaemia/reperfusion (I/R) injury. NEDD4-1 has been shown to positively regulate nuclear trafficking of the activated form of Akt. However, the role of NEDD4-1 in cardiac I/R injury remains to be elucidated. In the present study, Lentiviral vectors were constructed to overexpre...
T-LAK-cell-originated protein kinase (TOPK) is a PDZ-binding kinase (PBK) that was recently identified as a novel member of the mitogen-activated protein kinase (MAPK) family. It has been shown to play an important role in many cellular functions. However, its role in cardiac function remains unclear. Thus, we have herein explored the biological fu...
The present study aimed to evaluate the effect of the ethyl acetate fraction of P. reptans root (PEF) preconditioning on expressions of lncRNAs H19 and MIAT in H9C2 myoblasts I/R injury.
H9C2 cells were treated with different concentrations ranging from (10–400 µg/ml) of PEF for 24 h, followed by simulation of I/R condition. For I/R experiments, H9...
Ischemic preconditioning (IPC) is the most powerful endogenous cardioprotective form of cellular adaptation. However, the inhibitory or augmenting mechanism underlying cardioprotection via IPC remains largely unknown. Suppressor of cytokine signaling-3 (SOCS3) is a cytokine-inducible potent negative feedback regulator of the signal transducer and a...
Citations
... It is already well established that exosomes function across species, with human-derived exosomes protective in mice. 48,49 This indicates that they act either via a specific mechanism that is highly conserved F I G U R E 3 Representative images from the mPTP assay in HL-1 cells. HL-1 cardiomyocytes were pre-loaded with a quenching concentration of TMRM, then subject to repeated confocal scanning with a HeNe laser. ...
Myocardial infarction requires urgent reperfusion to salvage viable heart tissue. However, reperfusion increases infarct size further by promoting mitochondrial damage in cardiomyocytes. Exosomes from a wide range of different cell sources have been shown to activate cardioprotective pathways in cardiomyocytes, thereby reducing infarct size. Yet, it is currently challenging to obtain highly pure exosomes in quantities enough for clinical studies. To overcome this problem, we used exosomes isolated from CTX0E03 neuronal stem cells, which are genetically stable, conditionally inducible and can be produced on an industrial scale. However, it is unknown whether exosomes from neuronal stem cells may reduce cardiac ischaemia/reperfusion injury. In this study, we demonstrate that exosomes from differentiating CTX0E03 cells can reduce infarct size in mice. In an in vitro assay, these exosomes delayed cardiomyocyte mitochondrial permeability transition pore opening, which is responsible for cardiomyocyte death after reperfusion. The mechanism of MPTP inhibition was via gp130 signalling and the downstream JAK/STAT pathway. Our results support previous findings that exosomes from non‐cardiomyocyte‐related cells produce exosomes capable of protecting cardiomyocytes from myocardial infarction. We anticipate our findings may encourage scientists to use exosomes obtained from reproducible clinical‐grade stocks of cells for their ischaemia/reperfusion studies.
