RNA-sequencing analysis of Ly6Chi macrophage and Ly6Clo macrophage harvested from infarcted heart
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ABSTRACT:
PROVIDER: PRJNA473977 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7241777.fastq.gz | Fastqsanger.gz | |||
| SRR7241778.fastq.gz | Fastqsanger.gz |
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Project description:C57BL/6 J mice were subjected to ligation of the left anterior descending coronary artery. Ly6Chi macrophages and Ly6Clo macrophages were collected from infarcted hearts at 3 days after MI.
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Project description:Ly6Clow macrophages promote scar formation and prevent early infarct expansion after myocardial infarction (MI). Although CD4+ T cells influence the regulation of Ly6Clow macrophages after MI, the mechanism remains largely unknown. Here, we focused on IL-21 and uncovered its physiological relevance in post-MI hearts. CD4+ T cells harvested from the infarcted heart produce IL-21 upon stimulation, and IL-21 receptor was expressed on Ly6Clo macrophages in the infarcted heart. The survival rate after MI was significantly improved in IL-21-deficient mice compared with WT mice. Moreover, transcriptome analysis of infarcted heart tissue demonstrated that inflammation was persistent in WT mice compared with IL-21-deficient mice. The number of neutrophils was significantly decreased, whereas the number of Ly6Clow macrophages was significantly increased in IL-21-deficient mice. Consistently, IL-21 enhanced the apoptosis of Ly6Clow macrophages. Furthermore, RNA-seq analysis of Ly6Chi and Ly6Clo macrophages stimulated with or without IL-21 for 24 hours revealed that IL-21 induces inflammatory responses in both Ly6Chi and Ly6Clo macrophages. Finally, the treatment with IL-21 receptor Fc protein significantly increased the survival after MI. Thus, the deletion of IL-21 improves survival after MI by preventing Ly6Clo macrophage apoptosis.
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Project description:Monocytes comprise two major subsets, Ly6Chi classical monocytes and Ly6Clo non-classical monocytes. Notch2 signaling in Ly6Chi monocytes triggers transition to Ly6Clo monocytes, which require Nr4a1, Bcl6, Irf2 and Cebpb. By comparison, less is known about transcriptional requirements for Ly6Chi monocytes. We find transcription factor CCAAT/enhancer-binding protein alpha (C/EBPα) is highly expressed in Ly6Chi monocytes, but down-regulated in Ly6Clo monocytes. A few previous studies described the requirement of C/EBPα in the development of neutrophils and eosinophils. However, role of C/EBPα for in vivo monocyte development has not been understood. We deleted the Cebpa +37 kb enhancer in mice, eliminating hematopoietic expression of C/EBPα, reproducing the expected neutrophil defect. Surprisingly, we also discovered a severe and selective loss of Ly6Chi monocytes, while preserving Ly6Clo monocytes. We find that BM progenitors from Cebpa +37–/– mice rapidly progress through the cMoP stage to develop directly into Ly6Clo monocytes even in the absence of Notch2 signaling. These results identify a previously unrecognized role for C/EBPα in maintaining Ly6Chi monocyte identity.
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Project description:Two types of monocytes, inflammatory and patrolling, infiltrate the hearts in both human myocarditis and murine experimental autoimmune myocarditis (EAM) model. The fates and functions of these infiltrating monocytes governing the progression of heart failure remain unclear. Here, we created parabiotic EAM and naïve mice to show that cardiac inflammation facilitate monocyte-to-macrophage differentiation. Using a combination of flow cytometry, time lapsed imaging and transmission electron microscopy, we demonstrated in vitro that cardiac fibroblasts interact with monocytes and are instrumental in facilitating monocyte-to-macrophage differentiation. Moreover, IL-17A stimulated cardiac fibroblasts completely arrested Ly6Clo monocyte proliferation and inhibited both Ly6Chi and Ly6Clo monocyte-to-macrophage differentiation both in vitro and in vivo after intracardiac injections of monocytes into the hearts. Intriguingly, IL-17A signaling through cardiac fibroblasts also significantly downregulated Mer tyrosine kinase (MerTK) expressions on Ly6Chi monocyte-derived macrophages, thus jeopardizing their phagocytic abilities. Collectively, our results implicate divergent fates and functions of heart-infiltrating monocytes influenced by cardiac fibroblasts.
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Project description:To evaluate the consequences of RBP-J loss of function in blood monocyte subsets, we sequenced RNA of blood Ly6Chi monocyte and Ly6Clo monocyte from WT and RBP-Jfl/fl Lyz2-Cre mice.
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Project description:Ly6Clo monocytes are a myeloid subset that specializes in the surveillance of vascular endothelium. Ly6Clo monocytes have been shown to derive from Ly6Chi monocytes. Notch2 signaling has been implicated as a trigger for Ly6Clo monocyte development, but the basis for this effect is unclear. Here, we examined the impact of Notch2 signaling of myeloid progenitors on the development of Ly6Clo monocytes in vitro. Notch2 signaling induced by delta-like ligand 1 (DLL1) efficiently induced the transition of Ly6Chi TremL4– monocytes into Ly6Clo TremL4+ monocytes. We further discovered two additional transcriptional requirements for development of Ly6Clo monocytes. Deletion of Bcl6 from myeloid progenitors abrogated development of Ly6Clo monocyte development. IRF2 was also required for Ly6Clo monocyte development in a cell-intrinsic manner. DLL1-induced in vitro transition into Ly6Clo TremL4+ monocytes required IRF2 but unexpectedly could occur in the absence of Nur77 or Bcl6. These results imply a transcriptional hierarchy for these factors in controlling Ly6Clo monocyte development.
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Project description:Ly6Clo monocytes are a myeloid subset that specializes in the surveillance of vascular endothelium. Ly6Clo monocytes have been shown to derive from Ly6Chi monocytes. NOTCH2 signaling has been implicated as a trigger for Ly6Clo monocyte development, but the basis for this effect is unclear. Here, we examined the impact of NOTCH2 signaling of myeloid progenitors on the development of Ly6Clo monocytes in vitro. NOTCH2 signaling induced by delta-like ligand 1 (DLL1) efficiently induced the transition of Ly6Chi TREML4– monocytes into Ly6Clo TREML4+ monocytes. We further discovered two additional transcriptional requirements for development of Ly6Clo monocytes. Deletion of BCL6 from myeloid progenitors abrogated development of Ly6Clo monocytes. IRF2 was also required for Ly6Clo monocyte development in a cell-intrinsic manner. DLL1-induced in vitro transition into Ly6Clo TREML4+ monocytes required IRF2 but unexpectedly could occur in the absence of NUR77 or BCL6. These results imply a transcriptional hierarchy for these factors in controlling Ly6Clo monocyte development.
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Project description:mRNA expression profiles between Ym1+Ly6Chi monocytes and Ym1-Ly6Chi monocytes from LPS-treated mice were analyzed by RNA-sequencing
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Project description:Macrophage-specific alfa5 integrin signaling protects the infarcted heart from adverse remodeling, by stimulating angiogenesis
| PRJNA788538 | ENA
Project description:Ly6Clo monocytes are a myeloid subset that specializes in the surveillance of vascular endothelium. Ly6Clo monocytes have been shown to derive from Ly6Chi monocytes. Notch2 signaling has been implicated as a trigger for Ly6Clo monocyte development, but the basis for this effect is unclear. Here, we examined the impact of Notch2 signaling of myeloid progenitors on the development of Ly6Clo monocytes in vitro. Notch2 signaling induced by delta-like ligand 1 (DLL1) efficiently induced the transition of Ly6Chi TremL4– monocytes into Ly6Clo TremL4+ monocytes. We further discovered two additional transcriptional requirements for development of Ly6Clo monocytes. Deletion of Bcl6 from myeloid progenitors abrogated development of Ly6Clo monocyte development. IRF2 was also required for Ly6Clo monocyte development in a cell-intrinsic manner. DLL1-induced in vitro transition into Ly6Clo TremL4+ monocytes required IRF2 but unexpectedly could occur in the absence of Nur77 or Bcl6. These results imply a transcriptional hierarchy for these factors in controlling Ly6Clo monocyte development. This experiment compare RNA expression profiles between nonclassical monocytes and various cell types involved in their development.
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