Expression data from wound skin of WT and Spink7 KO mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE282599 | GEO | 2025/04/02
REPOSITORIES: GEO
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Project description:Wound healing, a multifaceted process, often leads to chronic wounds when disrupted. Predominantly, research in this area has relied on in vitro or animal models, which potentially oversimplify the intricacies of human wound healing. This simplification could contribute to the current gap in effective clinical therapies and prognostic tools. Our study aims to deepen the understanding of human skin wound healing mechanisms at the temporal protein level. Utilizing labeled mass spectrometry, we quantified the proteome of full-thickness skin samples at both acute and late healing stages from legs of 14 healthy individuals. Our results revealed distinct proteomic profiles corresponding to different wound healing days, indicating a unique protein signature for each stage. Functional enrichment analysis identified key elements such as post-translational modifications, histone interaction networks, and proteins related to transcription and metabolism as pivotal in the early phases of healing. Additionally, a comparative analysis of protein and mRNA expression in similar sample types revealed only moderate correlation, suggesting that mRNA assessments alone might not fully capture the complexity of the healing process. This finding underscores the necessity for multi-omics approaches to comprehensively understand complex molecular mechanisms such as human skin wound healing.
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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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Project description:Expression data from wound skin of WT and Spink7 KO mice
| PRJNA1189436 | ENA