02268nas a2200205 4500000000100000008004100001260001000042653002100052100001400073700001300087700001500100700001500115700001600130245009600146856009800242300001200340490000700352520168900359022001402048 2022 d bLepra10aGeneral Medicine1 aYuniati R1 aRiawan W1 aWidayati A1 aKhrisna MB1 aKristina TN00aHistopathology of SUMO in TGF-β1 signaling in neural lesions of leprosy reversal reactions uhttps://leprosyreview.org/admin/public/api/lepra/website/getDownload/6298a32fafaac119da731702 a138-1480 v933 a
Background Neural lesions are one of the main pathologies occurring in leprosy, which can result in devastating consequences due to disability and deformity. Transforming Growth Factor β (TGF-β) is important in the development of tissue fibrosis. The signaling process for TGF-β starts when it binds to TβRI and TβRII, activating and inducing the phosphorylation of Smad2 and Smad3. SUMOylation is a posttranslational modification, mediating the phosphorylation of Smad3 and regulating the TGF-β response. S100b is a marker of nerve damage. Objectives This study evaluates the in-vivo expression levels of SUMO-1 and SUMO2/3/4, the distribution of Schwann cells and mononuclear cells, and the distribution of S100b and collagen-1 in nerve biopsies of patients with leprosy reversal reactions. Methods Biopsies from twenty-six leprosy patients with reversal reactions (RR) and twenty-four leprosy patients without reversal reactions were stained for SUMO-1, SUMO-2/3/4, S100b, and collagen. We analyzed the cells using a Nikon microscope under 400× magnification. Results We found an increased distribution of SUMO-1, SUMO-2/3/4, macrophages, S100b, and collagen staining in neural lesions of reversal reaction patients, compared to leprosy patients without reversal reactions. Conclusion TGF-β plays an important role in the development of fibrosis in the neural lesions of patients with leprosy. Regulation of the transcription process is mediated by TGF-β1 signaling by SUMO-1 and/or SUMO-2/3/4. The increase in macrophages and collagen, with the decrease in S100b, in patients with neural lesions reflects the damage to nerves in leprosy reversal reactions.
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