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BACH1 orchestrates macrophage state transitions to coordinate regenerative inflammation [chimeric BMT]

ABSTRACT: To delineate the transcriptional changes, we used the cardiotoxin (CTX) acute muscle injury model and profiled the chromatin accessibility (ATAC-seq) and gene expression (RNA-seq) in sorted macrophage populations at different time-points during muscle regeneration. We identified BACH1 a heme-responsive transcriptional repressor, as a novel regulator of this process. Histological analysis reveals that Bach1 myeloid-specific knockout mice present a persistent necrotic fiber as well as delayed tissue repair while FACS and bulk RNA-seq show an abnormal macrophage phenotype switch and deregulation of critical genes involved in regenerative inflammation. To study how BACH1 affects the macrophage subtype specification and cellular composition during muscle repair, we have performed single-cell RNA-seq (scRNA-seq) experiments in control and myeloid specific Bach1 knockout models at different time points post CTX injury in mice. Our results indicate significant differences in the macrophage subsets composition and gene expression profiles demonstrated by the magnitude of expression of critical inflammatory and repair-related genes. In conclusion, by combining single-cell transcriptomics and macrophage-specific knockouts, we revealed a crucial role for BACH1 in regulating macrophage subtype specification and subsequently skeletal muscle regeneration.

ORGANISM(S): Mus musculus

PROVIDER: GSE294249 | GEO | 2026/05/31

REPOSITORIES: GEO

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BACH1 orchestrates macrophage state transitions to coordinate regenerative inflammation [Individualmouse]

Project description:To delineate the transcriptional changes, we used the cardiotoxin (CTX) acute muscle injury model and profiled the chromatin accessibility (ATAC-seq) and gene expression (RNA-seq) in sorted macrophage populations at different time-points during muscle regeneration. We identified BACH1 a heme-responsive transcriptional repressor, as a novel regulator of this process. Histological analysis reveals that Bach1 myeloid-specific knockout mice present a persistent necrotic fiber as well as delayed tissue repair while FACS and bulk RNA-seq show an abnormal macrophage phenotype switch and deregulation of critical genes involved in regenerative inflammation. To study how BACH1 affects the macrophage subtype specification and cellular composition during muscle repair, we have performed single-cell RNA-seq (scRNA-seq) experiments in control and myeloid specific Bach1 knockout models at different time points post CTX injury in mice. Our results indicate significant differences in the macrophage subsets composition and gene expression profiles demonstrated by the magnitude of expression of critical inflammatory and repair-related genes. In conclusion, by combining single-cell transcriptomics and macrophage-specific knockouts, we revealed a crucial role for BACH1 in regulating macrophage subtype specification and subsequently skeletal muscle regeneration.

2026-05-31 | GSE294248 | GEO

GSDME-controlled pyroptosis promotes muscle repair by coordinating tissue resident macrophages and fibro-adipogenic progenitors

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2026-01-05 | MTBLS10509 | MetaboLights

Expression data of CD11b+ cells isolated from WT and C3aR knockout mice after CTX injury

Project description:Regeneration of skeletal muscle following injury is accompanied by transient inflammation initiation and resolution. However, it is unclear what signals control these processes. To better understand the biological pathways by C3a-C3aR activation in monocyte druing muscle regeneration,we examined global transcriptional changes in macrophages from the muscle after CTX injury.Male C57BL/6J mice were used at 12 weeks of age. 30 ul 10uM Cardiotoxin (CTX) was injected to TA muscle to injury muscle. CD11b+ cells was isolated from WT and C3aR-/- muscle at 1 day after CTX injury by FACS , then total RNA obtained from these cells were used for the analysis of RNA-seq.

2017-08-31 | E-MTAB-5886 | biostudies-arrayexpress

GSDME-controlled pyroptosis promotes muscle repair by coordinating tissue resident macrophages and fibro-adipogenic progenitors [RNA-seq]

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Investigation of Bach1 function by heme-iron homeostasis in bone marrow derived macrophage

Project description:Macrophages are central in regulating iron homeostasis. Transcription repressor Bach1 regulates by heme. Here we investigated the relationship between heme-regulated Bach1 and bone marrow derived macrophage. We found that Bach1 KO macrophage showed that up-regulated genes were the process that iron-heme homeostasis and maintenance related gene compared with WT. Our results suggest that Bach1 expression is important to the heme homeostasis and maintenance in the bone marrow derived macrophage.

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Skewed macrophage polarization in aging skeletal muscle

Project description:Skeletal muscle aging is a major causative factor for disability and frailty in the elderly. Recent theories about the origins of the progressive impairment of skeletal muscle with aging emphasize a disequilibrium between damage and repair. Macrophages participate in muscle tissue repair first as pro-inflammatory M1 subtype and then as M2 anti-inflammatory subtype. However, information on macrophage presence in skeletal muscle is still sporadic and the effect of aging on different phenotypes remains unknown. In this study, we sought to characterize the polarization status of macrophages human skeletal muscle at different ages. We found that most macrophages in human skeletal muscle are M2, and that this number increased with advancing age. On the contrary, M1 macrophages decline with aging, making the total number of macrophages invariant with older age. Notably, M2 macrophages co-localized with increasing intermuscular adipose tissue (IMAT) in aging skeletal muscle. The mouse strain BALB/c, intrinsically M2-prone, showed increased IMAT and regenerating myofibers in skeletal muscle, accompanied by elevated expression of adipocyte markers and M2 cytokines. Collectively, we report that polarization of macrophages to the major M2 subtype is associated with IMAT, and propose that increased M2 in aged skeletal muscle may reflect active repair of aging-associated muscle damage.

2022-01-01 | GSE125481 | GEO

The transcriptome sequencing on muscle tissue from control group (CTX) and denervated group(CTX-DeN)

Project description:The transcriptome sequencing on muscle tissue from control group (CTX) and denervated group(CTX-DeN). The PI3K/Akt pathway is involved in denervation-aggravated muscle HO.

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Genome-wide map of BACH1 binding in HEK 293T cells

Project description:BTB and CNC homology 1 (BACH1) is a heme-binding transcription factor repressing the transcription from a subset of MAF recognition elements (MAREs) at low intracellular heme levels. Upon heme binding, BACH1 is released from the MAREs, resulting in increased expression of antioxidant response genes. To systematically address the gene regulatory networks involving BACH1, we combined chromatin immunoprecipitation-sequencing (ChIP-seq) analysis of BACH1 target genes in HEK 293 cells with knock-down of BACH1 using three independent types of small interfering RNAs followed by transcriptome profiling using microarrays. The 59 BACH1 target genes identified by ChIP-seq were found highly enriched in genes showing expression changes after BACH1 knock-down, demonstrating the impact of BACH1 repression on transcription. In addition to known and new BACH1 targets involved in heme degradation (HMOX1, FTL, FTH1, ME1, SLC48A1) and redox regulation (GCLC, GCLM, SLC7A11), we also discovered BACH1 target genes effecting cell cycle and apoptosis pathways (ITPR2, CALM1, SQSTM1, TFE3, EWSR1, CDK6, BCL2L11, MAFG) as well as subcellular transport processes (CLSTN1, PSAP, MAPT, vault RNA). The newly identified impact of BACH1 on genes involved in neurodegenerative processes and proliferation provides an interesting basis for future dissection of BACH1-mediated gene repression in neurodegeneration and virus-induced cancerogenesis. Examination of BACH1 binding in HEK 293T cells by chromatin immunoprecipitation-sequencing (CHIP-seq) with input DNA as control.

2011-05-13 | E-GEOD-28051 | biostudies-arrayexpress

Profiling of glycerol- and CTX-induced models of muscle regeneration in mice

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