Quantitation of Acute Necrosis After Experimental Myocardial Infarction

Yeap, Xin Yi; Dehn, Shirley; Adelman, Jeremy; Lipsitz, Jeremy; Thorp, Edward B.

doi:10.1007/978-1-62703-383-1_9

Cited by 20 publications

(14 citation statements)

References 18 publications

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“…Using the open‐chest in situ I/R model, 30 minutes of ischaemia were applied by occluding the left anterior descending (LAD) coronary artery followed by 2 hours of reperfusion in wild‐type (WT) and AOX littermates. The infarct size was estimated as a percentage scar tissue of the risk zone . As shown in Figure A,B, AOX expression did not confer any benefit.…”

Section: Resultsmentioning

confidence: 90%

“…The infarct size was estimated as a percentage scar tissue of the risk zone. 41,52 As shown in Figure 1A,B, AOX expression did not confer any benefit. We next sought to investigate whether the heart might nevertheless benefit during the early post-ischaemic phase through improved functional recovery of surviving myocytes and analysed heart contractile functions ex vivo in the isolated, perfused (Langendorff) heart.…”

Section: Aox Does Not Decrease Acute I/r Injuriesmentioning

confidence: 78%

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Respiratory chain signalling is essential for adaptive remodelling following cardiac ischaemia

Szibor

Schreckenberg

Gizatullina

et al. 2020

J Cellular Molecular Medi

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Cardiac ischaemia‐reperfusion (I/R) injury has been attributed to stress signals arising from an impaired mitochondrial electron transport chain (ETC), which include redox imbalance, metabolic stalling and excessive production of reactive oxygen species (ROS). The alternative oxidase (AOX) is a respiratory enzyme, absent in mammals, that accepts electrons from a reduced quinone pool to reduce oxygen to water, thereby restoring electron flux when impaired and, in the process, blunting ROS production. Hence, AOX represents a natural rescue mechanism from respiratory stress. This study aimed to determine how respiratory restoration through xenotopically expressed AOX affects the re‐perfused post‐ischaemic mouse heart. As expected, AOX supports ETC function and attenuates the ROS load in post‐anoxic heart mitochondria. However, post‐ischaemic cardiac remodelling over 3 and 9 weeks was not improved. AOX blunted transcript levels of factors known to be up‐regulated upon I/R such as the atrial natriuretic peptide (Anp) whilst expression of pro‐fibrotic and pro‐apoptotic transcripts were increased. Ex vivo analysis revealed contractile failure at nine but not 3 weeks after ischaemia whilst label‐free quantitative proteomics identified an increase in proteins promoting adverse extracellular matrix remodelling. Together, this indicates an essential role for ETC‐derived signals during cardiac adaptive remodelling and identified ROS as a possible effector.

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Section: Resultsmentioning

confidence: 90%

Section: Aox Does Not Decrease Acute I/r Injuriesmentioning

confidence: 78%

Respiratory chain signalling is essential for adaptive remodelling following cardiac ischaemia

Szibor

Schreckenberg

Gizatullina

et al. 2020

J Cellular Molecular Medi

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“…Reducing immigration of ΦIM into the heart and kidney after myocardial infarction and transplantation is associated with reduced tissue pathology (10, 42-44). Using a permanent left anterior descending artery occlusion model (45), we determined the impact of 3 days of PLGA-IMP treatment, initiated 12 hours after occlusion, by histopathology and immunohistochemistry 1 week after occlusion. One week after occlusion, vehicle-treated mice had a strong infiltration of monocytes into the myocardium, with up to 40% of the left ventricular wall involved (Fig.…”

Section: Resultsmentioning

confidence: 99%

Therapeutic Inflammatory Monocyte Modulation Using Immune-Modifying Microparticles

et al. 2014

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Inflammatory monocyte-derived effector cells play an important role in the pathogenesis of numerous inflammatory diseases. However, no treatment option exists that is capable of modulating these cells specifically. We show that infused negatively charged, immune-modifying microparticles (IMPs), derived from polystyrene, microdiamonds, or biodegradable poly(lactic-co-glycolic) acid, were taken up by inflammatory monocytes, in an opsonin-independent fashion, via the macrophage receptor with collagenous structure (MARCO). Subsequently, these monocytes no longer trafficked to sites of inflammation; rather, IMP infusion caused their sequestration in the spleen through apoptotic cell clearance mechanisms and, ultimately, caspase-3–mediated apoptosis. Administration of IMPs in mouse models of myocardial infarction, experimental autoimmune encephalomyelitis, dextran sodium sulfate–induced colitis, thioglycollate-induced peritonitis, and lethal flavivirus encephalitis markedly reduced monocyte accumulation at inflammatory foci, reduced disease symptoms, and promoted tissue repair. Together, these data highlight the intricate interplay between scavenger receptors, the spleen, and inflammatory monocyte function and support the translation of IMPs for therapeutic use in diseases caused or potentiated by inflammatory monocytes.

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“…After being photographed, the infarct areas and the area of left ventricular were calculated by the computer image analysis system. The percentage of infarction size was calculated according to the following formula: infarction size% = area of infarction size in left ventricular tissues/total area of left ventricular tissues × 100% (Yeap, Dehn, Adelman, Lipsitz, & Thorp, ).…”

Section: Methodsmentioning

confidence: 99%

“…infarction size% = area of infarction size in left ventricular tissues/ total area of left ventricular tissues × 100% (Yeap, Dehn, Adelman, Lipsitz, & Thorp, 2013).…”

mentioning

confidence: 99%

Annexin A3 gene silencing promotes myocardial cell repair through activation of the PI3K/Akt signaling pathway in rats with acute myocardial infarction

Meng

Zhang

et al. 2018

Journal Cellular Physiology

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Acute myocardial infarction (AMI), as a severe consequence of coronary atherosclerotic heart disease, always contributes to the loss of myocardial cells. Mounting evidence shows that annexin protects the myocardium from ischemic injury. In this study, we examine the inhibition of annexin A3 (ANXA3) on AMI through the phosphatidylinositide 3‐kinase/protein kinase B (PI3K/Akt) signaling pathway. We selected rats to build an AMI model which was then assigned into different groups. The hemodynamic parameters after transfection were detected by using enzyme‐linked immunosorbent assay. The effect of silencing of ANXA3 on inflammatory reaction and the PI3K/Akt signaling pathway was assessed. Rats transfected with ANXA3‐short hairpin RNA had alleviated hemodynamics, inflammatory reaction, decreased infarct size, α‐smooth muscle actin, Collagen I, and Collagen III as well as an increased vascular endothelial growth factor. Silencing ANAX3 would promote repair and healing of myocardial tissue by activation of the PI3K/Akt signaling pathway. Collectively, our study provides evidence that the downregulation of ANXA3 promotes the repair and healing of myocardial tissues by activating the PI3K/Akt signaling pathway.

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Quantitation of Acute Necrosis After Experimental Myocardial Infarction

Cited by 20 publications

References 18 publications

Respiratory chain signalling is essential for adaptive remodelling following cardiac ischaemia

Respiratory chain signalling is essential for adaptive remodelling following cardiac ischaemia

Therapeutic Inflammatory Monocyte Modulation Using Immune-Modifying Microparticles

Annexin A3 gene silencing promotes myocardial cell repair through activation of the PI3K/Akt signaling pathway in rats with acute myocardial infarction

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