ArticleEuropean journal of medical research2026
miR-194-5p-mediated suppression of protein tyrosine phosphatase non-receptor type 12 (PTPN12) expression in the thymus enhances immunologic functional restoration in aged mice.
Article in European journal of medical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveThis study aimed to explore the role of miR-194 in the post-transcriptional regulation of PTPN12 and its impact on age-related thymic atrophy.
methodsmiR-194-5p and PTPN12 expression levels in thymus tissues from young and aged mice were assessed using quantitative PCR and western blot analysis. An aged-mouse model was established to overexpress varying levels of miR-194-5p. Expression levels of PTPN12, AKT, BAX, p50, and p65 in thymic epithelial cells were analyzed via quantitative PCR and western blot. Flow cytometry was used to evaluate TEC cell cycle progression, proliferation, and apoptosis. CD4
resultsmiR-194 expression peaked in the thymus of middle-aged (6-7 months) C57BL/6 mice, while PTPN12 expression was highest in the young (1-2 months) mice and declined with age. TEC survival was enhanced in the miR-194-5p overexpression group, as indicated by cell cycle and apoptosis analyses. Additionally, CD4
conclusionThis study demonstrated that miR-194-5p modulates thymic immunological function in aged mice, highlighting its potential role in age-related thymic atrophy.
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