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Scar management through modulation of the fibrotic microenvironment by CAR-Trem2-macrophages

ABSTRACT: Scar management through modulation of the fibrotic microenvironment by CAR-Trem2-macrophages

PROVIDER: PRJNA1045715 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26963388_1.fastq.gz	Fastqsanger.gz
	SRR26963388_2.fastq.gz	Fastqsanger.gz
	SRR26963389_1.fastq.gz	Fastqsanger.gz
	SRR26963389_2.fastq.gz	Fastqsanger.gz
	SRR26963390_1.fastq.gz	Fastqsanger.gz

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Scar management through modulation of the fibrotic microenvironment by CAR-Trem2-macrophages

Project description:Dipeptidyl peptidase 4 (Dpp4) plays a pivotal role in fibrotic and nonfunctional scar development following skin injury and is present in a subset of fibroblasts implicated in scar formation. Simultaneously, heterogeneous vascular endothelial cells (ECs) retain their capacity to drive tissue regeneration and repair within scarred areas. Effective strategies for inhibiting scar-associated fibroblasts and regulating EC subtypes in the scar microenvironment remain unclear. Here, we engineered CAR-Trem2-Ms capable of targeting DPP4+ fibroblasts and modulating EC phenotypes within the scar microenvironment to effectively prevent and treat scarring. Furthermore, compared to those in normal control samples, DPP4 expression levels were higher in both clinical scar databases and samples from scar patients. We transferred a CAR gene specifically targeting Dpp4+ fibroblasts into macrophages, which were then induced into CAR-Trem2-Ms with 1,25-dihydroxycholecalciferol (an active form of VD, VD3). Hydrogel micropore microneedles (mMNs) were employed to deliver CAR-Trem2-Ms to effectively alleviate scar formation. Single-cell transcriptome sequencing and analysis revealed that CAR-Trem2-Ms could modify EC phenotypes and regulate fibrosis by suppressing the profibrotic gene Lrg1. CAR-Trem2-Ms effectively inhibited fibrosis in fibroblasts induced by high EC LRG1 expression in vitro, further revealing the underlying mechanism by which CAR-Trem2-Ms exert their antifibrotic effects. Our findings offer a promising approach for treating post-traumatic scarring and provide novel insights into the pathological mechanisms underlying fibrosis.

2024-09-24 | GSE248759 | GEO

Scar management through modulation of the fibrotic microenvironment by CAR-Trem2-macrophages (scRNA-seq)

2024-09-24 | GSE248960 | GEO

Scar management through modulation of the fibrotic microenvironment by CAR-Trem2-macrophages (scRNA-seq)

Project description:Scar management through modulation of the fibrotic microenvironment by CAR-Trem2-macrophages (scRNA-seq)

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SCAR

Project description:Drosophila melanogaster SCAR, SCAR, is differentially expressed in 8 experiment(s);

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SCAR

Project description:Drosophila melanogaster SCAR, SCAR, is expressed in 2 baseline experiment(s);

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car

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Midkine-a regulates the formation of a fibrotic scar during zebrafish heart regeneration

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TREM2 regulates microglial cell activation in response to demyelination in vivo

Project description:Microglia are phagocytic cells that survey the brain and perform neuroprotective functions in response to tissue damage, but their activating receptors are largely unknown. Triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial immunoreceptor whose loss-of-function mutations in humans cause presenile dementia, while genetic variants are associated with increased risk of neurodegenerative diseases. In myeloid cells, TREM2 has been involved in the regulation of phagocytosis, cell proliferation and inflammatory responses in vitro. However, it is unknown how TREM2 contributes to microglia function in vivo. Here, we identify a critical role for TREM2 in the activation and function of microglia during cuprizone (CPZ)-induced demyelination. TREM2-deficient (TREM2(-/-)) mice had defective clearance of myelin debris and more axonal pathology, resulting in impaired clinical performances compared to wild-type (WT) mice. TREM2(-/-) microglia proliferated less in areas of demyelination and were less activated, displaying a more resting morphology and decreased expression of the activation markers MHC II and inducible nitric oxide synthase as compared to WT. Mechanistically, gene expression and ultrastructural analysis of microglia suggested a defect in myelin degradation and phagosome processing during CPZ intoxication in TREM2(-/-) microglia. These findings place TREM2 as a key regulator of microglia activation in vivo in response to tissue damage. Two STAGE (6weeks 12 weeks),

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Microarray profiling analysis of microRNAs expression in Hypertrophic scar

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