Peer-reviewed veterinary case report
Hypoxic ADSC Exosomes Alleviate Primary Sjögren's Syndrome-Induced Skin Injury via GLRX2 Delivery and Ferroptosis Suppression.
- Journal:
- Immunological investigations
- Year:
- 2025
- Authors:
- Wang, Xin et al.
- Affiliation:
- Department of Rheumatology and Immunology · China
- Species:
- rodent
Abstract
BACKGROUND: The aim of the present study was to assess the therapeutic effects of ADSC-Exos for SS-induced skin injury. METHODS: A mouse model of SS was constructed and Exos from ADSCs (Exos) and hypoxia-pretreated ADSCs (HExos) were isolated. The therapeutic effects of Exos were identified using an enzyme-linked immunosorbent assay, immunohistochemistry, and immunofluorescence. High-throughput sequencing (HTS) was employed to identify differentially expressed genes between ADSC-Exos and ADSC-HExos. The results showed that treatment with ADSC-Exos, especially ADSC-HExos, inhibited SS-induced expression of inflammatory factors, ferroptosis, and deposition of reactive oxygen species. RESULTS: The results of HTS and polymerase chain reaction analysis revealed that GLRX2 plays an important role in protected effects of ADSC-HExo against SS-induced skin injury.analysis usingHaCaT cells confirmed that GLRX2 inhibited lipopolysaccharide-induced skin injury by inhibiting ferroptosis, as confirmed with the ferroptosis inhibitorFerrostatin-1. GLRX2 upregulation increased the therapeutic effects of ADSC-Exos against skin injury of SS mice. CONCLUSION: Moreover,ADSC-HExos effectively promoted collagen I expression, suggesting that ADSC-HExos attenuated primary SS-induced skin injury via GLRX2 delivery and ferroptosis suppression.
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Search related cases →Original publication: https://pubmed.ncbi.nlm.nih.gov/40492693/