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Pro-inflammatory macrophages impair skeletal muscle regeneration in ischemic-damaged limbs by inducing precocious differentiation of satellite cells [RNA-seq]

ABSTRACT: To validate the findings from scRNA-seq, we purified CD11b+/F480+ macrophages by FACS from the hind limb muscle of C57BL/6 (n=3) and BALB/c (n=2) mice at 3-days post HLI for bulk RNA-seq analysis We then performed gene expression profiling analysis using data obtained from RNA-seq of isolated macrophages from C57BL/6 and BALB/c mice at day 3 after HLI surgery.

ORGANISM(S): Mus musculus

PROVIDER: GSE227076 | GEO | 2023/10/16

REPOSITORIES: GEO

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Pro-inflammatory macrophages impair skeletal muscle regeneration in ischemic-damaged limbs by inducing precocious differentiation of satellite cells [scRNA-seq]

Project description:To investigate the molecular mechanisms responsible for failed skeletal muscle repair in the Chronic limb threatening ischemia (CLTI) limb. We used single cell RNA sequencing (scRNA-seq) to profile the transcriptomes of the skeletal muscle specimens.

2023-10-16 | GSE227075 | GEO

Endothelial cells control muscle regeneration through angiocrine lactate

Project description:We studied metabolic angiocrine mechanisms by which endothelial cell_ECs_ can contribute to muscle regeneration from ischemia by using endothelial specific pfkfb3 knockout mice_pfkfb3DEC_ after hind-limb ischemia_HLI_. During muscle regeneration, monocytes are recruited to the injured area and rapidly become macrophages which initially exhibit a more pro-inflammatory M1-like phenotype but soon thereafter functionally repolarize towards an M2-like phenotype to actively support muscle regeneration. Interestingly, macrophages derived from pfkfb3DEC failed to polarized to M2-like macrophages after HLI. Reduced macrophage polarization impairs angiogenesis and muscle regeneration. The RNAseq data are pfkfb3DEC and pfkfb3WT muscle derived macrophages 3 days after HLI.

2020-05-18 | GSE148584 | GEO

Pro-inflammatory macrophages impair skeletal muscle regeneration in ischemic-damaged limbs by inducing precocious differentiation of satellite cells [scRNA-seq]

Project description:Pro-inflammatory macrophages impair skeletal muscle regeneration in ischemic-damaged limbs by inducing precocious differentiation of satellite cells [scRNA-seq]

| PRJNA943182 | ENA

Pro-inflammatory macrophages impair skeletal muscle regeneration in ischemic-damaged limbs by inducing precocious differentiation of satellite cells [RNA-seq]

Project description:Pro-inflammatory macrophages impair skeletal muscle regeneration in ischemic-damaged limbs by inducing precocious differentiation of satellite cells [RNA-seq]

| PRJNA943181 | ENA

Skeletal muscle regeneration failure in ischemic-damaged limbs is associated with pro-inflammatory macrophages and premature differentiation of satellite cells.

Project description:BackgroundChronic limb-threatening ischemia (CLTI), a severe manifestation of peripheral arterial disease (PAD), is associated with a 1-year limb amputation rate of approximately 15-20% and substantial mortality. A key feature of CLTI is the compromised regenerative ability of skeletal muscle; however, the mechanisms responsible for this impairment are not yet fully understood. In this study, we aim to delineate pathological changes at both the cellular and transcriptomic levels, as well as in cell-cell signaling pathways, associated with compromised muscle regeneration in limb ischemia in both human tissue samples and murine models of CLTI.MethodsWe performed single-cell transcriptome analysis of ischemic and non-ischemic muscle from the same CLTI patients and from a murine model of CLTI. In both datasets, we analyzed gene expression changes in macrophage and muscle satellite cell (MuSC) populations as well as differential cell-cell signaling interactions and differentiation trajectories.ResultsSingle-cell transcriptomic profiling and immunofluorescence analysis of CLTI patient skeletal muscle demonstrated that ischemic-damaged tissue displays a pro-inflammatory macrophage signature. Comparable results were observed in a murine CLTI model. Moreover, integrated analyses of both human and murine datasets revealed premature differentiation of MuSCs to be a key feature of failed muscle regeneration in the ischemic limb. Furthermore, in silico inferences of intercellular communication and in vitro assays highlight the importance of macrophage-MuSC signaling in ischemia induced muscle injuries.ConclusionsCollectively, our research provides the first single-cell transcriptome atlases of skeletal muscle from CLTI patients and a murine CLTI model, emphasizing the crucial role of macrophages and inflammation in regulating muscle regeneration in CLTI through interactions with MuSCs.

| S-EPMC10636829 | biostudies-literature

Single cell RNA-sequencing of pleural cavity macrophages naïve and nematode-infected C57BL/6 and BALB/c mice

Project description:The recent revolution in tissue-resident macrophage biology has resulted largely from murine studies performed in the C57BL/6 strain. Here, we provide a comprehensive analysis of immune cells in the pleural cavity using both C57BL/6 and BALB/c mice. Unlike C57BL/6 mice, naïve tissue-resident Large Cavity Macrophages (LCM) of BALB/c mice failed to fully implement the tissue residency programme. Following infection with a pleural-dwelling nematode these pre-existing differences were accentuated with LCM expansion occurring in C57BL/6 but not BALB/c mice. While infection drove monocyte recruitment in both strains, only in C57BL/6 mice were monocytes able to integrate into the resident pool. Monocyte to macrophage conversion required both T cells and IL-4Rα signalling. Host genetics are therefore a key influence on tissue resident macrophage biology, and during nematode infection Th2 cells control the differentiation pathway of tissue resident macrophages.

2022-09-01 | GSE189031 | GEO

Genetic variation in IL-4 activated tissue resident macrophages alters the epigenetic state to determine strain specific synergistic responses to LPS [Hi-C]

Project description:IL-4 activates tissue resident macrophages (TRMs) to mediate tissue repair and clearance of nematode infections in mice, but most studies have been performed on the C57BL/6 background. The natural genetic variation between C57BL/6 and BALB/c mouse strains can result in differences in allergic responses, parasite resistance, monocyte to macrophage conversion and response to IL-4 activation. Here, we investigated in vivo IL-4 activation in TRMs of the peritoneal cavity from C57BL/6 and BALB/c mice and find that C57BL/6 TRMs are surprisingly more transcriptionally responsive to IL-4 stimulation, with greater association of induced genes with super enhancers, induced enhancers and topologically associating domains (TAD) boundaries. IL-4-directed epigenomic remodeling showed NF-κB motif enrichment only in C57BL/6 TRMs. This resulted in an enhanced synergistic response upon in vitro lipopolysaccharide (LPS) exposure in IL-4 activated C57BL/6 TRMs but not for BALB/c, despite unstimulated BALB/c TRMs having a stronger transcriptional response to LPS than C57BL/6 TRMs. Single cell RNA sequencing (scRNAseq) analysis of mixed bone marrow chimeric mice indicates that transcriptional differences between C57BL/6 and BALB/c TRMs is cell intrinsic within the same tissue environment. Hence, genetic variation alters IL-4-induced cell intrinsic epigenetic reprogramming between C57BL/6 and BALB/c TRMs to regulate the magnitude of synergistic responses to LPS exposure.

2023-12-29 | GSE248029 | GEO

Genetic variation in IL-4 activated tissue resident macrophages alters the epigenetic state to determine strain specific synergistic responses to LPS [ChIP-seq]

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Genetic variation in IL-4 activated tissue resident macrophages alters the epigenetic state to determine strain specific synergistic responses to LPS [scRNA-seq]

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Genetic variation in IL-4 activated tissue resident macrophages alters the epigenetic state to determine strain specific synergistic responses to LPS [scATAC-seq]

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