Pretreatment of Exosomes Derived from hUCMSCs with LPS Ameliorates Liver Fibrosis by Inhibiting the Smad3C Through Upregulating MiR-126 in the HSC-T6 Cell Line

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Cheraghzadeh Maryam; Matour Emad; Kabizadeh Benyamin; Shakerian Elham; Rashidi Mojtaba

مرکز اطلاعات علمی Scientific Information Database (SID) - Trusted Source for Research and Academic Resources

Journal Paper

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Journal: Hepatitis Monthly Year:2023 | Volume:23 | Issue:1 Page(s): 1-10

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Title

Pretreatment of Exosomes Derived from hUCMSCs with LPS Ameliorates Liver Fibrosis by Inhibiting the Smad3C Through Upregulating MiR-126 in the HSC-T6 Cell Line

Author(s)

Keywords

HSC-T6 Line

MSC-Ex

TGF-β-SMAD3c

LPS

Liver Fibrosis

Abstract

Background: Activated hepatic stellate cells (HSC) through the TGF-β signaling pathway are likely to exacerbate Liver Fibrosis, which is a later stage of NASH, a condition in which, in addition to HSC activation, the overexpression of extracellular matrix (ECM) proteins, specifically collagen-I α and α-SMA, is expected. MicroRNA-126a, a modulator of HSC activation, influences the phosphorylation of Smad2/3. Objectives: This study aimed to investigate the impact of exosomes on miRNAs implicated in the progression of Liver Fibrosis by focusing on the role of miR-126a in the HSC-T6 cell line. Methods: In the present study, we investigated the effects of exosomes derived from LPS-stimulated mesenchymal stem cells (MSCs) on the expression of miR-126a and the phosphorylation of Smad3c in the HSC-T6 cell line. First, HSC-T6 cells were cultured in DMEM supplemented with 10% FBS. Next, we isolated exosomes derived from MSCs using the ExoCib kit. Finally, we examined the gene expression levels of collagen-Iα, α-SMA, and miR-126a using real-time PCR. Results: The results showed that treatment with TGFβ1 increased the phosphorylation of p-Smad3c (P < 0.0001), as well as the expression of α-SMA and Collagen-Iα. Conversely, miR-126a expression was down-regulated after treatment with TGFβ1 (P < 0.01). However, exposure to LPS-treated MSC-derived exosomes resulted in a significant decrease in the levels of p-Smad3c phosphorylation (P < 0.001) and the gene expression of α-SMA and Collagen-Iα, accompanied by the up-regulation of miR-126a (P < 0.05). Conclusions: Based on our observations, MSCs-derived exosomes were able to reduce the expression of the genes associated with hepatic fibrosis, such as collagen-Iα and α-SMA. Furthermore, exosomes inhibited Smad3c phosphorylation by increasing miR-126a expression, ultimately hindering the progression of Liver Fibrosis. Therefore, exosomes should be recognized as a valuable and beneficial therapeutic tool for Liver Fibrosis.

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