Diffuse Lung Disease: Diffuse Lung Disease: Connective Tissue Disease |

Role of miR-146a Modulation in Human Mesenchymal Stem Cells for Counteraction of Pulmonary Fibrosis FREE TO VIEW

Ming Liu, PhD; Yansheng Wang, PhD; Lixia Zheng, MS; Jun Xu, MD
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Guangzhou Institute of Respiratory Diseases, Guangzhou, China

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;149(4_S):A208. doi:10.1016/j.chest.2016.02.215
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SESSION TITLE: Diffuse Lung Disease: Connective Tissue Disease

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM

PURPOSE: Pulmonary fibrosis is a lethal and progressive disorder with no effective therapies. Recent studies have shown that MSCs have immunomodulatory and tissue-protective properties that allow them to manipulate the local environment of the injured tissue, ameliorating the inflammation and promoting repair. However, the mechanisms for anti-fibrosis are still not fully understood.

METHODS: MSCs isolated from bone marrow (BM), umbilical cord (UC), amniotic fluid (AF) were cultured. Their morphological characteristic, immunological features, anti-fibrosis efficency and miR expression profiles were investigated and compared, then MSCs were transfected with miR-146a mimic or miR-146a inhibitor to investigation of the role of miR-146a modulation in MSCs-mediated anti-inflammatory and anti-fibrotic effects in vitro and in Bleomycin-induced pulmonary fibrosis mouse model.

RESULTS: In this study, we found that MSCs derived from different sources have distinct anti-fibrotic efficacy. MSCs-BM shows more efficacies in treating pulmonary fibrosis, which is associated with a low level of miR-146a expression. Down and up regulation the expression of miR-146a in MSC could induce an enhanced and decreased immunosuppressive and anti-fibrotic effect of MSCs on pulmonary fibrosis through targeting to PGES2 and STAT1 decreases the production of PGE2 and IP-10.

CONCLUSIONS: Mir-146a can regulate the treatment efficacy of MSC in pulmonary fibrosis through targeting PGE2 and IP-10.

CLINICAL IMPLICATIONS: These findings contribute to our understanding of the immunoregulatory and tissue-protective properties of MSCs, which may lead to better application of MSCs in pulmonary fibrosis treatment.

DISCLOSURE: The following authors have nothing to disclose: Ming Liu, Yansheng Wang, Lixia Zheng, Jun Xu

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