{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE325nnn/GSE325404/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE325404"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"FAP-derived CCL2 is required for adequate monocyte/macrophage infiltration to support acute skeletal muscle injury repair","description":"Repair of acutely injured skeletal muscle relies on an adequate inflammatory response predominated by monocyte/macrophage infiltration. The process requires injured muscles to produce C-C chemokine ligand 2 (CCL2). The present study identified fibro/adipogenic progenitors (FAPs) as the primary source of CCL2 in acutely injured muscle where the pro-inflammatory subcluster of FAPs expanded rapidly and expressed the highest level of CCL2. FAP-specific deletion of Ccl2 largely abolished CCL2 production by acutely injured muscle, reducing monocyte/macrophage infiltration and impairing muscle regeneration. In vitro, the CCL2 expression by both mouse and human FAPs were induced by danger signal-containing muscle homogenates through toll-like receptor signaling. The CCL2 expression by mouse FAPs was also induced by infiltrating neutrophils partly through their secretion of pro-inflammatory cytokines. Our findings suggest an important immune sentinel role for FAPs, as they sense muscle damage, produce CCL2 to recruit inflammatory MOs, and promote injury repair.progression of dystrophic muscle in Duchenne muscular dystrophy (DMD) patients and DMD mouse model mdx5cv mice. The cellular and molecular mechanism underlying this difference has yet to be fully elucidated. To this end, the present study compared the single-cell transcriptomes of intramuscular monocytes/macrophages from uninjured and acutely injured quadriceps of 14 weeks-old wild-typed (WT) mice, and from quadriceps and diaphragm of age-matched mdx5cv mice, using single cell-based RNA sequencing (scRNA-seq) analysis. Our results identified multiple functionally diverse monocyte/macrophage clusters co-existing in each injured muscle sample. Both Ly6Chi and Ly6Clo intramuscular monocytes/macrophages were heterogenous, containing different clusters among different injury conditions. These clusters did not conform to strict M1/M2 activation, and were involved differentially in inflammation, extracellular matrix (ECM) remodeling, and myogenesis during skeletal muscle injury repair. These findings uncovered the heterogeneity of monocyte/macrophage activation in both acutely injured and dystrophic skeletal muscle, shedding light on the molecular and cellular mechanisms underlying the differential roles of monocytes/macrophages in acute skeletal muscle injury and muscular dystrophy in DMD.","dates":{"publication":"2026/06/29"},"accession":"GSE325404","cross_references":{"GSM":["GSM9602554","GSM9602553"],"GPL":["24247"],"GSE":["325404"],"taxon":["Mus musculus"]}}