scholarly journals Telomerase expression confers cardioprotection in the adult mouse heart after acute myocardial infarction

2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Christian Bär ◽  
Bruno Bernardes de Jesus ◽  
Rosa Serrano ◽  
Agueda Tejera ◽  
Eduard Ayuso ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Adult Mouse ◽  
Mouse Heart

scholarly journals S100a8/a9 Signaling Causes Mitochondrial Dysfunction and Cardiomyocyte Death in Response to Ischemic/Reperfusion Injury

Circulation ◽  
2019 ◽  
Vol 140 (9) ◽  
pp. 751-764 ◽  
Author(s):  
Yulin Li ◽  
Boya Chen ◽  
Xinying Yang ◽  
Congcong Zhang ◽  
Yao Jiao ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Percutaneous Coronary Intervention ◽  
Cardiovascular Events ◽  
Ischemia Reperfusion ◽  
Coronary Intervention ◽  
Major Adverse Cardiovascular Events ◽  
Mouse Heart ◽  
Early Reperfusion ◽  
Percutaneous Coronary

Background: Myocardial ischemia-reperfusion (MI/R) injury is a significant clinical problem without effective therapy. Unbiased omics approaches may reveal key MI/R mediators to initiate MI/R injury. Methods: We used a dynamic transcriptome analysis of mouse heart exposed to various MI/R periods to identify S100a8/a9 as an early mediator. Using loss/gain-of-function approaches to understand the role of S100a8/a9 in MI/R injury, we explored the mechanisms through transcriptome and functional experiment. Dynamic serum S100a8/a9 levels were measured in patients with acute myocardial infarction before and after percutaneous coronary intervention. Patients were prospectively followed for the occurrence of major adverse cardiovascular events. Results: S100a8/a9 was identified as the most significantly upregulated gene during the early reperfusion stage. Knockout of S100a9 markedly decreased cardiomyocyte death and improved heart function, whereas hematopoietic overexpression of S100a9 exacerbated MI/R injury. Transcriptome/functional studies revealed that S100a8/a9 caused mitochondrial respiratory dysfunction in cardiomyocytes. Mechanistically, S100a8/a9 downregulated NDUF gene expression with subsequent mitochondrial complex I inhibition via Toll-like receptor 4/Erk–mediated Pparg coactivator 1 alpha/nuclear respiratory factor 1 signaling suppression. Administration of S100a9 neutralizing antibody significantly reduced MI/R injury and improved cardiac function. Finally, we demonstrated that serum S100a8/a9 levels were significantly increased 1 day after percutaneous coronary intervention in patients with acute myocardial infarction, and elevated S100a8/a9 levels were associated with the incidence of major adverse cardiovascular events. Conclusions: Our study identified S100a8/a9 as a master regulator causing cardiomyocyte death in the early stage of MI/R injury via the suppression of mitochondrial function. Targeting S100a8/a9-intiated signaling may represent a novel therapeutic intervention against MI/R injury. Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT03752515

scholarly journals Cardiomyocyte proliferation and progenitor cell recruitment underlie therapeutic regeneration after myocardial infarction in the adult mouse heart

2013 ◽  
Vol 5 (2) ◽  
pp. 191-209 ◽  
Author(s):  
Konstantinos Malliaras ◽  
Yiqiang Zhang ◽  
Jeffrey Seinfeld ◽  
Giselle Galang ◽  
Eleni Tseliou ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Progenitor Cell ◽  
Adult Mouse ◽  
Mouse Heart ◽  
Cardiomyocyte Proliferation ◽  
Cell Recruitment

scholarly journals Circulating E3 ligases are novel and sensitive biomarkers for diagnosis of acute myocardial infarction

2015 ◽  
Vol 128 (11) ◽  
pp. 751-760 ◽  
Author(s):  
Qiu-Yue Han ◽  
Hong-Xia Wang ◽  
Xiao-Hong Liu ◽  
Cai-Xia Guo ◽  
Qi Hua ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Time Course ◽  
Troponin I ◽  
Expression Patterns ◽  
Pcr Analysis ◽  
Mouse Heart ◽  
Roc Curve Analysis ◽  
Similar Time ◽  
E3 Ligases

Ubiquitin ligase (E3) is a decisive element of the ubiquitin-proteasome system (UPS), which is the main pathway for intracellular protein turnover. Recently, circulating E3 ligases have been increasingly considered as cancer biomarkers. In the present study, we aimed to determine if cardiac-specific E3 ligases in circulation can serve as novel predictors for early diagnosis of acute myocardial infarction (AMI). By screening and verifying their tissue expression patterns with microarray and real-time PCR analysis, six of 261 E3 ligases, including cardiac-specific Rnf207 and cardiac- and muscle-enriched Fbxo32/atrogin-1, Trim54/MuRF3, Trim63/MuRF1, Kbtbd10/KLHL41, Asb11 and Asb2 in mouse heart, were selected for the present study. In the AMI rats, the levels of five E3 ligases including Rnf207, Fbxo32, Trim54, Trim63 and Kbtbd10 in the plasma were significantly increased compared with control animals. Especially, the plasma levels of Rnf207 was markedly increased at 1 h, peaked at 3 h and decreased at 6–24 h after ligation. Further evaluation of E3 ligases in AMI patients confirmed that plasma Rnf207 level increased significantly compared with that in healthy people and patients without AMI, and showed a similar time course to that in AMI rats. Simultaneously, plasma level of cardiac troponin I (cTnI) was measured by ELISA assays. Finally, receiver operating characteristic (ROC) curve analysis indicated that Rnf207 showed a similar sensitivity and specificity to the classic biomarker troponin I for diagnosis of AMI. Increased cardiac-specific E3 ligase Rnf207 in plasma may be a novel and sensitive biomarkers for AMI in humans.

scholarly journals Conditional Transgenic Expression of Fibroblast Growth Factor 9 in the Adult Mouse Heart Reduces Heart Failure Mortality After Myocardial Infarction

Circulation ◽  
2011 ◽  
Vol 123 (5) ◽  
pp. 504-514 ◽  
Author(s):  
Mortimer Korf-Klingebiel ◽  
Tibor Kempf ◽  
Klaus-Dieter Schlüter ◽  
Christian Willenbockel ◽  
Torben Brod ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Adult Mouse ◽  
Mouse Heart ◽  
Fibroblast Growth ◽  
Transgenic Expression

scholarly journals GALECTIN-1, A GALACTOSIDE BINDING LECTIN WITH IMMUNOMODULATORY EFFECTS, IS UPREGULATED IN THE MOUSE HEART DURING ACUTE MYOCARDIAL INFARCTION

2010 ◽  
Vol 55 (10) ◽  
pp. A123.E1147
Author(s):  
Ignacio M. Seropian ◽  
Stefano Toldo ◽  
Diego O. Croci ◽  
Antonio Abbate ◽  
Gabriel A. Rabinovich ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Mouse Heart ◽  
Immunomodulatory Effects ◽  
Binding Lectin

scholarly journals Mitochondrial Calcium Flux Contributes to Arrhythmia in Mouse Heart during Acute Myocardial Infarction

2017 ◽  
Vol 112 (3) ◽  
pp. 131a
Author(s):  
An Xie ◽  
Hong Liu ◽  
Anyu Zhou ◽  
Guangbin Shi ◽  
Samuel C. Dudley
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Calcium Flux ◽  
Mitochondrial Calcium ◽  
Mouse Heart

scholarly journals Single-cell transcriptome analyses reveal novel targets modulating cardiac neovascularization by resident endothelial cells following myocardial infarction

2019 ◽  
Vol 40 (30) ◽  
pp. 2507-2520 ◽  
Author(s):  
Ziwen Li ◽  
Emmanouil G Solomonidis ◽  
Marco Meloni ◽  
Richard S Taylor ◽  
Rodger Duffin ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Endothelial Cells ◽  
Single Cell ◽  
Adult Mouse ◽  
Bone Marrow Cells ◽  
Lineage Tracing ◽  
Border Region ◽  
Mouse Heart ◽  
Ischaemic Injury ◽  
Mesenchymal Transition

AbstractAimsA better understanding of the pathways that regulate regeneration of the coronary vasculature is of fundamental importance for the advancement of strategies to treat patients with heart disease. Here, we aimed to investigate the origin and clonal dynamics of endothelial cells (ECs) associated with neovascularization in the adult mouse heart following myocardial infarction (MI). Furthermore, we sought to define murine cardiac endothelial heterogeneity and to characterize the transcriptional profiles of pro-angiogenic resident ECs in the adult mouse heart, at single-cell resolution.Methods and resultsAn EC-specific multispectral lineage-tracing mouse (Pdgfb-iCreERT2-R26R-Brainbow2.1) was used to demonstrate that structural integrity of adult cardiac endothelium following MI was maintained through clonal proliferation by resident ECs in the infarct border region, without significant contributions from bone marrow cells or endothelial-to-mesenchymal transition. Ten transcriptionally discrete heterogeneous EC states, as well as the pathways through which each endothelial state is likely to enhance neovasculogenesis and tissue regeneration following ischaemic injury were defined. Plasmalemma vesicle-associated protein (Plvap) was selected for further study, which showed an endothelial-specific and increased expression in both the ischaemic mouse and human heart, and played a direct role in regulating human endothelial proliferation in vitro.ConclusionWe present a single-cell gene expression atlas of cardiac specific resident ECs, and the transcriptional hierarchy underpinning endogenous vascular repair following MI. These data provide a rich resource that could assist in the development of new therapeutic interventions to augment endogenous myocardial perfusion and enhance regeneration in the injured heart.

scholarly journals Aromatase Inhibition Attenuates Desflurane-Induced Preconditioning against Acute Myocardial Infarction in Male Mouse Heart In Vivo

PLoS ONE ◽  
2012 ◽  
Vol 7 (8) ◽  
pp. e42032 ◽  
Author(s):  
Virginija Jazbutyte ◽  
Jan Stumpner ◽  
Andreas Redel ◽  
Johan M. Lorenzen ◽  
Norbert Roewer ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Male Mouse ◽  
Mouse Heart ◽  
Aromatase Inhibition
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