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ScRNA-seq of mouse cardiac CD45+ cells with CITE-seq and cell Hashing II

ABSTRACT: We performed scRNA-seq and CITE-seq of CD45+ cells extracted from the steady state mouse heart, and at 5 days after myocardial infarction in wildtype and Trem2 deficient mice

ORGANISM(S): Mus musculus

PROVIDER: GSE197853 | GEO | 2022/07/21

REPOSITORIES: GEO

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scRNA-seq of mouse cardiac CD45+ cells with CITE-seq and cell Hashing

Project description:We performed scRNA-seq and CITE-seq of CD45+ cells extracted from the steady state mouse heart, and at 5 days after myocardial infarction with or without depletion of CCR2+ cells

2022-07-21 | GSE197441 | GEO

scRNA-seq of mouse CD45+ aortic cells with CITE-seq and cell Hashing after continuous or alternate diet

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Trem2 Macrophage Promote Cardiac Repair in Myocardial Infarction via Efferocytosis and Carbohydrate Metabolism

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CD45+ vs CD45- RCC proteome characterization

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Single cell 5’ transcript, TCRαβ enriched, and Cell hashing/CITE-seq library preparation on the 10x chromium, and sequencing

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2022-03-02 | E-MTAB-9455 | biostudies-arrayexpress

scRNA-seq of total mouse aortic cells with CITE-seq and cell Hashing

Project description:We performed single-cell RNA-seq analysis with CITE-seq and cell hashing of total viable aortic cells from Ldlr-/- mice fed a high fat diet for 13 weeks

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Mouse Cardiac Fibroblasts post MI

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The effect of insulin-like growth factor 1 treatment on cardiac myeloid cells 3 days post-myocardial infarction

Project description:To test the mechanism by which IGF1 is cardioprotective, we performed single cell RNA sequencing on myeloid cells isolated from the heart 3 days after myocardial infarction of mice with and without IGF1 treatment. Myocardial infarction was induced in C57Bl6/J mice by 45 min occlusion of the left anterior descending artery followed by 3 days of reperfusion. Animals of the IGF1 group (n=3) received 40 ng/g mature recombinant IGF1 subcutaneously as bolus at the beginning of reperfusion. In addition, IGF1 (1 µg/g/d) was administered continuously during reperfusion using micro-osmotic pumps (Alzet, 1003D) that were implanted subcutaneously. Control mice received vehicle (0.1% BSA). After 3 days hearts were digested and CD45+CD11b+ cells were isolated using FACS cell sorting. Each sample contained cells containing 1 control and 1 IGF1 treated mouse, labeled with TotalSeq hashtags. 16000 cells were used as input for the single-cell droplet libraries generation for each sample.

2023-12-31 | E-MTAB-11590 | biostudies-arrayexpress

Cardiac-specific YAP activation improve cardiac function and survival in an experimental murine MI model

Project description:In this study, we used a cardiac-specific, inducible expression system to activate YAP in adult mouse heart. Activation of YAP in adult heart promoted cardiomyocyte proliferation and did not deleteriously affect heart function. Furthermore, YAP activation after myocardial infarction (MI) preserved heart function and reduced infarct size. Using adeno-associated virus subtype 9 (AAV9) as a delivery vector, we expressed human YAP in the murine myocardium immediately after MI. We found that AAV9:hYAP significantly improved cardiac function and mouse survival. AAV9:hYAP did not exert its salutary effects by reducing cardiomyocyte apoptosis. Rather, we found that AAV9:hYAP stimulated adult cardiomyocyte proliferation. Gene expression profiling indicated that AAV9:hYAP stimulated cell cycle gene expression, enhanced TGFβ-signaling, and activated of components of the inflammatory response.Cardiac specific YAP activation after MI mitigated myocardial injury after MI, improved cardiac function and mouse survival. These findings suggest that therapeutic activation of hYAP or its downstream targets, potentially through AAV-mediated gene therapy, may be a strategy to improve outcome after MI. Three groups were involved in this study: sham group, AAV9:Luci+MI group and AAV9-YAP+MI group. Each group contained three biological replicates. The sham group had neither myocardial infarction nor AAV injection. The AAV9:Luci +MI(L for brief) group had myocardial infarction and injected with AAV9:Luic. The AAV9:hYAP+MI(YAP for brief) group had myocardial infarction and injected with AAV9:hYAP. 5 days after MI and AAV injection, the heart apexes were collected and the total RNA were isolated for microarray analysis.

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Immune profiling of murine cardiac leukocytes identifies Trem2 as a novel mediator of hypertensive heart failure

Project description:Heart failure with preserved ejection fraction (HFpEF) is characterized by diastolic dysfunction, microvascular dysfunction and myocardial fibrosis with recent evidence implicating the immune system in orchestrating cardiac remodeling. Here, we show the mouse model of deoxycorticosterone acetate (DOCA)-salt hypertension induces key elements of HFpEF, including diastolic dysfunction, exercise intolerance, and pulmonary congestion in the setting of preserved ejection fraction. CITE-Seq analysis of cardiac immune cells reveals an altered abundance and/or transcriptional signature in multiple cell types, most notably cardiac macrophages. The DOCA-salt model results in differential expression of several known and novel genes in cardiac macrophages, including upregulation of Trem2, which was also recently implicated in obesity and atherosclerosis. The role of macrophage Trem2 in cardiac remodeling, however, is unknown. We found that mice with genetic deletion of Trem2 exhibit increased cardiac hypertrophy and decreased cardiac capillary density after DOCA-salt treatment compared to wild-type controls, and Trem2-deficient macrophages have impaired expression of pro-angiogenic gene programs. Furthermore, we found that plasma levels of soluble TREM2 are elevated in human heart failure. Together, our data suggest a novel cardioprotective role for macrophage Trem2 in cardiac remodeling and heart failure and provide an atlas for the identification of additional targets that can lead to improved diagnostic and therapeutic strategies for HFpEF.

2023-05-01 | GSE211166 | GEO

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