Systemic sclerosis (SSc) is an autoimmune disorder that affects multiple organs. It is characterized by a thickening of the dermis and connective tissue caused by collagen accumulation, and vascular injuries that induce hypoxia. The present study investigated the therapeutic potential of bone marrow-derived mesenchymal stem cells (BMSCs) expressing thioredoxin 1 (Trx-1) in treating SSc-mediated skin disease after transplantation into a bleomycin-induced murine model. Mice with bleomycin-induced SSc were subcutaneously injected with BMSCs or Trx-1-overexpressing BMSCs and exposed to hypoxic conditions for 48 hours. Two weeks later, skin tissue samples were collected to assess fibrosis, oxidative stress, and angiogenesis by western blotting, ELISA, and histologic and immunofluorescence approaches. In vivo experiments showed that Trx-1-overexpressing BMSCs inhibited hypoxia-induced apoptosis and inhibited fibrosis under hypoxic conditions, possibly by downregulating transforming growth factor-β. Trx-1-overexpressing BMSCs also promoted the formation of tubular-like structures by endothelial progenitor cells, indicating that Trx-1 can promote angiogenesis in bleomycin-induced SSc. These results demonstrate that the transplantation of Trx-1-overexpressing BMSCs restored normal skin tissue in a mouse model of bleomycin-induced SSc, highlighting the therapeutic potential of engineered BMSCs for treating SSc.
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BackgroundAtopic eczema (AE) is a chronic relapsing inflammatory skin disease. The objective of this study was to identify key genes related to the development of AE.MethodsThe GSE6012 dataset was obtained from the Gene Expression Omnibus (GEO) database. The limma package was used to analyze differentially expressed genes (DEGs). Then, the weighted gene co-expression network analysis (WGCNA) package was utilized to generate weighted correlation networks of up- and downregulated genes. Additionally, the WGCNA package was used for enrichment analyses to explore the underlying functions of DEGs in modules (weighted correlation sub-networks) significantly associated with AE.ResultsA total of 515 DEGs were identified between lesional and non-lesional skin samples. For the upregulated genes, the blue module was found to have a significant positive correlation with AE. Importantly, small proline-rich protein 2C (SPRR2C) and defensin, beta 4A (DEFB4A) exhibited higher |log fold change (FC)| values and were the key nodes of the network. Moreover, KEGG pathway analysis revealed that the upregulated genes in the blue module were primarily involved in cytokine-cytokine receptor interaction. Additionally, for the downregulated genes, the brown module was found to have a significant positive correlation with AE. Further, WNT inhibitory factor 1 (WIF1), cryptochrome 2 (CRY2), and keratin 19 (KRT19) had higher |log FC| values and were key nodes of the network.ConclusionSPRR2C, DEFB4A, WIF1, CRY2, KRT19 and cytokine-cytokine receptor interaction might be correlated with the development of AE.
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