The miR-130a-3p/TGF-βRII Axis Participates in Inhibiting the Differentiation of Fibroblasts Induced by TGF-β1

Pulmonary fibrosis (PF) is a chronic progressive interstitial lung disease that has a poor prognosis. Abnormal activation of transforming growth factor-β1 (TGF-β1) plays a crucial role in fibroblast differentiation. Mesenchymal stem cells (MSCs) are currently being considered for the treatment of PF...

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Main Authors: Yanhong Liu, Yan Ding, Yapeng Hou, Tong Yu, Hongguang Nie, Yong Cui
Format: Article
Language:English
Published: Frontiers Media S.A. 2021-07-01
Series:Frontiers in Pharmacology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fphar.2021.732540/full
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author Yanhong Liu
Yan Ding
Yapeng Hou
Tong Yu
Hongguang Nie
Yong Cui
author_facet Yanhong Liu
Yan Ding
Yapeng Hou
Tong Yu
Hongguang Nie
Yong Cui
author_sort Yanhong Liu
collection DOAJ
description Pulmonary fibrosis (PF) is a chronic progressive interstitial lung disease that has a poor prognosis. Abnormal activation of transforming growth factor-β1 (TGF-β1) plays a crucial role in fibroblast differentiation. Mesenchymal stem cells (MSCs) are currently being considered for the treatment of PF, but the regulatory mechanisms are poorly understood. We co-cultured bone marrow-derived MSCs and mouse lung fibroblasts (MLg) in the presence of TGF-β1, and studied the protein/mRNA expression of fibrosis markers and related signaling pathways. The effects of miR-130a-3p and TGF-β receptor II (TGF-βRII) on the differentiation of MLg induced by TGF-β1 were studied using immunofluorescence assay, Western blot, and quantitative real-time PCR techniques, respectively. Our results showed that MSCs reversed the overexpression of fibrosis markers and TGF-β1/Smad signaling pathway proteins and mRNAs after TGF-β1 treatment and increased the level of miR-130a-3p. TGF-βRII was identified as a target of miR-130a-3p and was evaluated by dual-luciferase reporter assay. The miR-130a-3p/TGF-βRII axis could suppress the differentiation of lung fibroblasts via the TGF-β1/Smad signaling pathway, thereby reducing the process of PF.
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spelling doaj.art-63a31c7dedac4e3ebc29a182aaaf279a2022-12-21T18:49:38ZengFrontiers Media S.A.Frontiers in Pharmacology1663-98122021-07-011210.3389/fphar.2021.732540732540The miR-130a-3p/TGF-βRII Axis Participates in Inhibiting the Differentiation of Fibroblasts Induced by TGF-β1Yanhong Liu0Yan Ding1Yapeng Hou2Tong Yu3Hongguang Nie4Yong Cui5Department of Stem Cells and Regenerative Medicine, College of Basic Medical Science, China Medical University, Shenyang, ChinaDepartment of Stem Cells and Regenerative Medicine, College of Basic Medical Science, China Medical University, Shenyang, ChinaDepartment of Stem Cells and Regenerative Medicine, College of Basic Medical Science, China Medical University, Shenyang, ChinaDepartment of Stem Cells and Regenerative Medicine, College of Basic Medical Science, China Medical University, Shenyang, ChinaDepartment of Stem Cells and Regenerative Medicine, College of Basic Medical Science, China Medical University, Shenyang, ChinaDepartments of Anesthesiology, The First Hospital of China Medical University, Shenyang, ChinaPulmonary fibrosis (PF) is a chronic progressive interstitial lung disease that has a poor prognosis. Abnormal activation of transforming growth factor-β1 (TGF-β1) plays a crucial role in fibroblast differentiation. Mesenchymal stem cells (MSCs) are currently being considered for the treatment of PF, but the regulatory mechanisms are poorly understood. We co-cultured bone marrow-derived MSCs and mouse lung fibroblasts (MLg) in the presence of TGF-β1, and studied the protein/mRNA expression of fibrosis markers and related signaling pathways. The effects of miR-130a-3p and TGF-β receptor II (TGF-βRII) on the differentiation of MLg induced by TGF-β1 were studied using immunofluorescence assay, Western blot, and quantitative real-time PCR techniques, respectively. Our results showed that MSCs reversed the overexpression of fibrosis markers and TGF-β1/Smad signaling pathway proteins and mRNAs after TGF-β1 treatment and increased the level of miR-130a-3p. TGF-βRII was identified as a target of miR-130a-3p and was evaluated by dual-luciferase reporter assay. The miR-130a-3p/TGF-βRII axis could suppress the differentiation of lung fibroblasts via the TGF-β1/Smad signaling pathway, thereby reducing the process of PF.https://www.frontiersin.org/articles/10.3389/fphar.2021.732540/fullpulmonary fibrosismesenchymal stem cellsmouse lung fibroblastmicroRNATGF-β1
spellingShingle Yanhong Liu
Yan Ding
Yapeng Hou
Tong Yu
Hongguang Nie
Yong Cui
The miR-130a-3p/TGF-βRII Axis Participates in Inhibiting the Differentiation of Fibroblasts Induced by TGF-β1
Frontiers in Pharmacology
pulmonary fibrosis
mesenchymal stem cells
mouse lung fibroblast
microRNA
TGF-β1
title The miR-130a-3p/TGF-βRII Axis Participates in Inhibiting the Differentiation of Fibroblasts Induced by TGF-β1
title_full The miR-130a-3p/TGF-βRII Axis Participates in Inhibiting the Differentiation of Fibroblasts Induced by TGF-β1
title_fullStr The miR-130a-3p/TGF-βRII Axis Participates in Inhibiting the Differentiation of Fibroblasts Induced by TGF-β1
title_full_unstemmed The miR-130a-3p/TGF-βRII Axis Participates in Inhibiting the Differentiation of Fibroblasts Induced by TGF-β1
title_short The miR-130a-3p/TGF-βRII Axis Participates in Inhibiting the Differentiation of Fibroblasts Induced by TGF-β1
title_sort mir 130a 3p tgf βrii axis participates in inhibiting the differentiation of fibroblasts induced by tgf β1
topic pulmonary fibrosis
mesenchymal stem cells
mouse lung fibroblast
microRNA
TGF-β1
url https://www.frontiersin.org/articles/10.3389/fphar.2021.732540/full
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