Project description:The left anterior descending coronary artery permanent ligation model of myocardial infarction was used to study the time of day differences in genetic responses post-MI between sleep-time MI, wake-time MI, wake-sham and sleep-sham mouse hearts. The micorarray approach allows the investigation of gene expression changes of all genes in sleep-time MI vs. wake-time MI vs. sham hearts.

2018-08-06 | GSE71906 | GEO

Mus musculus

Project description:Expression data from C57BL/6J and MRL/MpJ hearts following acute myocardial infarction

| PRJNA120865 | ENA

E-GEOD-19322

Project description:Expression data from C57BL/6J and MRL/MpJ hearts following acute myocardial infarction

2015-09-15 | E-GEOD-19322 | ExpressionAtlas

Evaluating the effects of cardiac telomerase re-activation after myocardial infarction in adult mice

Project description:Coronary heart disease is a main cause of death in the developed world and treatment success remains modest with high mortality rates within one year after myocardial infarction (MI). Thus, new therapeutic targets and effective treatments are necessary. Short telomeres are risk factors for age-associated diseases including heart disease. Here, we address the potential of telomerase (Tert) activation in prevention of heart failure after MI in adult mice. We use adeno-associated viruses for cardiac-specific Tert expression in a mouse model of MI. We find that upon MI, hearts expressing Tert show attenuated cardiac dilation, improved ventricular function and smaller infarct scars concomitant with increased mouse survival by 17% compared to controls. Furthermore, Tert treatment results in elongated telomeres, increased numbers of Ki67 and pH3-positive cardiomyocytes and a gene expression switch towards a regeneration signature of neonatal mice. Our work highlights telomerase activation as a novel therapeutic strategy to prevent heart failure after MI. Mice of one year of age were left untreated (control) or injected with 5*10^11 adeno associated viruses particles of serotype 9 (AAV9) that carry either en empty expression cassette or express telomerase under control of the CMV promoter. Virus injected mice then underwent myocardial infarction induced through permenant left anterior descending artery (LAD) ligation. Mice that survived for six weeks after LAD ligation were sacrificed and 4 hearts per group (AAV9-empty or AAV9-Tert) and 3 control hearts (no virus treatment, no ligation) were subjected to total RNA isolation for micro array analysis.

2014-12-15 | E-GEOD-62973 | biostudies-arrayexpress

Pitx2 promotes heart repair by transcriptionally activating the antioxidant response after cardiac injury

Project description:Myocardial infarction results in compromised myocardial function with heart failure due to insufficient cardiomyocyte self-renewal. Unlike lower vertebrates, mammalian hearts only have a transient neonatal renewal capacity. Reactivating the primitive reparative ability in the fully mature heart requires an intimate knowledge of the molecular mechanisms promoting early heart repair. Here we identified a novel factor that can sufficiently promote heart muscle repair. By screening an established Hippo-deficient heart regeneration model for renewal promoting factors, we found that PITX2 protein expression in ventricles was induced after cardiomyocyte injury. Moreover, Pitx2-deficient neonatal hearts failed to repair after apex resection. Pitx2-gain-of-function in ventricular cardiomyocytes conferred reparative ability to the adult mouse heart after myocardial infarction. Integrated genomic analyses indicated that Pitx2 activated genes encoding electron transport chain components and reactive oxygen species scavengers. Pitx2 mutant myocardium had elevated reactive oxygen species levels while supplement of antioxidants suppressed the Pitx2-loss-of-function phenotype. Furthermore, PITX2 directly binds NFE2L2 and translocates from cytoplasm to nucleus upon oxidative stress.

2016-05-19 | GSE70413 | GEO

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