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Interleukin 13 Signaling to Macrophages Promotes Functional Recovery after Myocardial Infarction

ABSTRACT: Interleukin 13 Signaling to Macrophages Promotes Functional Recovery after Myocardial Infarction

PROVIDER: PRJNA967327 | ENA |

REPOSITORIES: ENA

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Interleukin 13 Signaling to Macrophages Promotes Functional Recovery after Myocardial Infarction

Project description:Adult mice were subjected to surgical myocardial infarction (MI), and daily injected with recombinant IL13 or PBS as a control following MI. Mice were euthanized at 4 or 7 days post injury and live leukocytes were isolated from the heart and subjected single cell RNA sequencing.

2024-01-24 | GSE231707 | GEO

Effect of senolytics (Navitoclax, ABT263) on recovery following Myocardial Infarction

Project description:Ischemia reperfusion injury (IRI) following intervention for myocardial infarction remains an unmet clinical problem. Using an established mouse model, we demonstrated that IRI induces multiple cardiac cell linages to senescence. Senescence is is detrimental to recovery, as treatment with the senolytic navitoclax improves functional recovery.Here we are using SWATH-MS to investigate the molecular mechanisms responsible for the effect of navitoclax treatment.

2020-02-29 | MSV000085040 | MassIVE

LncRNAs and mRNAs changes in border zone of myocardial infarction in rats

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2024-05-03 | PXD043448 | Pride

myocardial infarction in Reg3beta knock-out mice

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2015-06-29 | E-MTAB-2561 | biostudies-arrayexpress

Altered gene expression pattern in peripheral blood mononuclear cells in patients with acute myocardial infarction

Project description:Despite a substantial progress in diagnosis and therapy, acute myocardial infarction (MI) is a major cause of mortality in the general population. A novel insight into the pathophysiology of myocardial infarction obtained by studying gene expression should help to discover novel biomarkers of MI and to suggest novel strategies of therapy. The aim of our study was to establish gene expression patterns in leukocytes from acute myocardial infarction patients. ST-segment elevation myocardial infarction alters expression of several groups of genes. On admission, several genes and pathways that could be directly or indirectly linked with lipid/glucose metabolism, platelet function and atherosclerotic plaque stability were affected (signaling of PPAR, IL-10, IL-6). Analysis at discharge highlighted specific immune response (upregulation of immunoglobulins). Highly significant and substantial upregulation of SOCS3 and FAM20 genes expression in the first 4-6 days of myocardial infarction in all patients is the most robust observation of our work Twenty-eight patients with ST-segment elevation myocardial infarction (STEMI) were included. The blood was collected on the 1st day of myocardial infarction, after 4-6 days, and after 6 months. Control group comprised 14 patients with stable coronary artery disease (CAD), without history of myocardial infarction. Gene expression analysis was performed with Affymetrix GeneChipM-BM-. Human Gene 1.0 ST microarrays and GCS3000 TG system.

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CCN3 administration after surgically induced myocardial infarction

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