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| Status |
Public on Aug 28, 2023 |
| Title |
Single cell RNAseq profiling of Tbx1 function in adult post myocardial infarction hearts [scRNA-seq] |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by high throughput sequencing
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| Summary |
Post-myocardial infarction (Post-MI) heart failure is an unanswered clinical challenge. Current immunological intervention trials to reduce MI damage are unsatisfactory. Thus a thorough understanding of post-MI immune response is imperative. Tbx1, the major 22q11.2 deletion syndrome (22q11.2DS) disease gene, reactivated in cardiac lymphatic endothelial cells (LECs) to promote post-MI repair. Endothelial deletion of Tbx1 deteriorated post-MI cardiac function through a dual approach, impaired lymphangiogenesis and weakened immunosuppression. To characterize cell autonous function of Tbx1 in endothelial population and cell non-autonous effect in immune cells, we set to performed scRNA-seq on Ctrl (Tbx1flox/flox) and Tbx1cko (Fabp4-Cre;Tbx1flox/flox) hearts. The dataset is comprised of total 55,106 single cells transcriptomes. We identified eight principal non-myocyte types with their known markers, including CD31-expressing vascular endothelial cell (VEC), LEC, pericyte, as well as CD45-expressing monocyte/macrophage, dendritic cell (DC), neutrophil, T/innate lymphoid cell (ILC), and B cell. Interestingly, we found that the relative percentage of monocyte/macrophage population, which is most abundant among all immune cells, was significantly decreased in Tbx1cko hearts, whereas T/ILC population was increased. Taken together, single cell transcriptomic analyses suggest a potential cell non-autonomous effect that Tbx1 deficiency in endothelium may cause imbalance in immune response.
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| Overall design |
We set to performed scRNA-seq on enriched CD31+ endothelial cells and CD45+ leucocytes from Ctrl and Tbx1cko hearts. We collected samples at 4, 5, 6, and 7 dpMI, reasoning that the the most significant cellular and transcriptional distincts between Ctrl and Tbx1cko would occur during the initial 4-day window of Tbx1 reactivation.
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| Contributor(s) |
Wang W, Li X, Zhang M, Zhang Z |
| Citation(s) |
37625409 |
| Submission date |
Sep 03, 2019 |
| Last update date |
Aug 29, 2023 |
| Contact name |
Min Zhang |
| E-mail(s) |
minzhang_scmc_heart@outlook.com
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| Organization name |
Shanghai Jiao Tong University School of Medicine
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| Department |
Shanghai Children's Medical Center
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| Lab |
Zhen Zhang
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| Street address |
1678 Dongfang Road
|
| City |
Shanghai |
| State/province |
Shanghai |
| ZIP/Postal code |
200127 |
| Country |
China |
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| Platforms (2) |
| GPL23479 |
BGISEQ-500 (Mus musculus) |
| GPL24247 |
Illumina NovaSeq 6000 (Mus musculus) |
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| Samples (8)
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| This SubSeries is part of SuperSeries: |
| GSE137064 |
Tbx1 promotes neo-lymphangiogenesis and constraints the immune response to facilitate repair. |
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| Relations |
| BioProject |
PRJNA563619 |
| SRA |
SRP220124 |
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