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Mol Biol Rep ; 51(1): 635, 2024 May 10.
Artículo en Inglés | MEDLINE | ID: mdl-38727850

RESUMEN

BACKGROUND: Psoriasis, a chronic inflammatory skin disease, is increasingly effectively managed with the targeted immunotherapy; however, long-term immunotherapy carries health risks, and loss of response. Therefore, we need to develop the alternative treatment strategies. Mesenchymal stem/stromal cell (M.S.C.) exosomes stand out for their remarkable immunomodulatory properties, gaining widespread recognition. This study investigated whether M.S.C. exosomes can reduce psoriasis-induced hyperplasia by inducing Transforming Growth Factor beta 2 (TGF-beta2) signaling. METHODOLOGY: Exosomes were isolated from M.S.C.s by ultracentrifugation. Then, scanning electron microscopy was used for the morphology of exosomes. To ascertain the exosome concentration, the Bradford test was used. To ascertain the cellular toxicity of exosomes in Human Umbilical Vein Endothelial Cells ( H.U.V.E.C), an MTT experiment was then conducted. Real-time PCR was used to quantify TGF beta2 expression levels, whereas an ELISA immunosorbent assay was used to determine the protein concentration of TGF beta2. RESULTS: In this study, the exosomes of 15-30 nm in size that were uniform, and cup-shaped were isolated. Moreover, the IC50 value for this Treatment was calculated to be 181.750 µg/ml. The concentration of TGF-ß2 gene in the target cells significantly increased following Treatment with the exosomes. Furthermore, the expression level of the studied gene significantly increased due to the Treatment. CONCLUSION: Upregulating the expression of TGF-ß2 in psoriatic cells via TGF-ß2 signaling is one way exosomes can help reduce hyperplasia.


Asunto(s)
Exosomas , Células Endoteliales de la Vena Umbilical Humana , Hiperplasia , Células Madre Mesenquimatosas , Psoriasis , Factor de Crecimiento Transformador beta2 , Exosomas/metabolismo , Células Madre Mesenquimatosas/metabolismo , Psoriasis/metabolismo , Humanos , Factor de Crecimiento Transformador beta2/metabolismo , Hiperplasia/metabolismo , Células Endoteliales de la Vena Umbilical Humana/metabolismo , Transducción de Señal , Animales
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