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Human Single Cell Transcriptional Profiling Identifies Epigenetically Altered PGE2 Pathway that Modulates Diabetic Macrophage Phenotype and Wound Repair

ABSTRACT: Human Single Cell Transcriptional Profiling Identifies Epigenetically Altered PGE2 Pathway that Modulates Diabetic Macrophage Phenotype and Wound Repair

PROVIDER: PRJNA646693 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12235469_1.fastq.gz	Fastqsanger.gz
	SRR12235469_2.fastq.gz	Fastqsanger.gz
	SRR12235470_1.fastq.gz	Fastqsanger.gz
	SRR12235470_2.fastq.gz	Fastqsanger.gz
	SRR12235471_1.fastq.gz	Fastqsanger.gz

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Human Single Cell Transcriptional Profiling Identifies Epigenetically Altered PGE2 Pathway that Modulates Diabetic Macrophage Phenotype and Wound Repair

Project description:single cell RNA-sequencing to profile the transcriptomes of lesional skin of diabetic patients at the cellular level.

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Sprayable Nanozyme Hydrogel Epigenetically Reprograms Inflammation for Diabetic Wound Regeneration [ATAC-seq]

Project description:Chronic diabetic wounds present a critical clinical challenge due to persistent inflammation and compromised healing. Here we report a novel sprayable nanozyme hydrogel that epigenetically reprograms macrophages to suppress inflammation and coordinate regeneration. Ultrasmall copper-based nanozymes (CuNZ, ~4 nm) synthesized via an eco-friendly one-pot method demonstrated potent multi-radical scavenging activity. When integrated into gelatin methacryloyl (Gel), CuNZ@Gel exhibited excellent sprayability, conformal skin coverage, and long-term storage stability, offering substantial translatable potential. Notably, the nanozyme hydrogel induced distinct epigenetic modifications in macrophages by remodeling chromatin accessibility, effectively shifting gene expression from pro-inflammatory to anti-inflammatory profiles. This epigenetic modulation persisted under oxidative stress, actively suppressing inflammatory while facilitating regenerative responses. In diabetic wound models, CuNZ@Gel significantly accelerated healing through its coordinated antioxidant, anti-inflammatory, and pro-regenerative actions. Unlike conventional passive dressings, our sprayable nanozyme hydrogel proactively reprograms the wound microenvironment via epigenetic antioxidant mechanisms, offering novel insights and strategy for managing chronic diabetic wounds and inflammatory skin complications.

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Sprayable Nanozyme Hydrogel Epigenetically Reprograms Inflammation for Diabetic Wound Regeneration [GeoMX spatial transcriptomics]

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Sprayable Nanozyme Hydrogel Epigenetically Reprograms Inflammation for Diabetic Wound Regeneration [mRNA-seq]

Project description:Sprayable Nanozyme Hydrogel Epigenetically Reprograms Inflammation for Diabetic Wound Regeneration [mRNA-seq]

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Sprayable Nanozyme Hydrogel Epigenetically Reprograms Inflammation for Diabetic Wound Regeneration [ATAC-seq]

Project description:Sprayable Nanozyme Hydrogel Epigenetically Reprograms Inflammation for Diabetic Wound Regeneration [ATAC-seq]

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Sprayable Nanozyme Hydrogel Epigenetically Reprograms Inflammation for Diabetic Wound Regeneration [Chip-seq]

Project description:Sprayable Nanozyme Hydrogel Epigenetically Reprograms Inflammation for Diabetic Wound Regeneration [Chip-seq]

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SFRP2 modulates functional phenotype transition and energy metabolism of macrophages during diabetic wound healing [Skin wound]

Project description:Diabetic foot ulcer (DFU) is a serious complication of diabetes mellitus, which causes great health damage and economic burden to patients. The pathogenesis of DFU is not fully understood.We screened wound healing-related genes using bioinformatics analysis, and full-thickness skin injury mice model and cellular assays were used to explore the role of target genes in diabetic wound healing. SFRP2 was identified as a wound healing-related gene, and the expression of SFRP2 is associated with immune cell infiltration in DFU. In vivo study showed that suppression of SFRP2 delayed the wound healing process of diabetic mice, impeded angiogenesis and matrix remodeling, and increased macrophage infiltration in wound tissues. In addition, suppression of SFRP2 enhanced M1 polarization in both the early and later stage of wound healing, and decreased M2 polarization in the later stage, which impeded the transition of M1 to M2 polarization of wound healing. Moreover, suppression of SFRP2 affected the transcriptome signatures-related to inflammatory response and energy metabolism at the early stage of wound healing. Extracellular flux analysis (EFA) showed that suppression of SFRP2 decreased mitochondrial energy metabolism and increased glycolysis in injury-related macrophages. Furthermore, suppression of SFRP2 inhibited transcriptome signaturesrelated to carbohydrate metabolism, lipid metabolism and amino acid metabolism, which consists the three main components of energy metabolism of macrophages. In conclusions, SFRP2 may function as a wound healing-related gene in DFU, and suppression of SFRP2 impaired diabetic wound healing by compromising the M1-to-M2 transition of macrophages and modulating the balance between mitochondrial energy metabolism and glycolysis.

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