Inhibition of bleomycin‐induced pulmonary fibrosis by bone marrow‐derived mesenchymal stem cells might be mediated by decreasing MMP9, TIMP‐1, INF‐γ and TGF‐β. (15th July 2015)

• Record Type: Journal Article
• Authors: Yu, Shi‐huan; Liu, Li‐jie; Lv, Bin; Che, Chun‐li; Fan, Da‐ping; Wang, Li‐feng; Zhang, Yi‐mei
• Is Part Of: Cell biochemistry and function. Volume 33:Number 6(2015:Aug.)
• Page Start: 356
• Page End: 365
• Publication Date: 2015-07-15
• Subjects: Cytochemistry -- Periodicals; Cell metabolism -- Periodicals; Biochemistry -- Periodicals; Cytology -- Periodicals; 572
• DOI: 10.1002/cbf.3118
• Languages: English
• ISSNs: 0263-6484

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <p>The study was aimed to investigate the mechanism and administration timing of bone marrow‐derived mesenchymal stem cells (BMSCs) in bleomycin (BLM)‐induced pulmonary fibrosis mice. Thirty‐six mice were divided into six groups: control group (saline), model group (intratracheal administration of BLM), day 1, day 3 and day 6 BMSCs treatment groups and hormone group (hydrocortisone after BLM treatment). BMSCs treatment groups received BMSCs at day 1, 3 or 6 following BLM treatment, respectively. Haematoxylin and eosin and Masson staining were conducted to measure lung injury and fibrosis, respectively. Matrix metalloproteinase (MMP9), tissue inhibitor of metalloproteinase‐1 (TIMP‐1), <italic>γ</italic>‐interferon (INF‐<italic>γ</italic>) and transforming growth factor <italic>β</italic>1 (TGF‐<italic>β</italic>) were detected in both lung tissue and serum. Histologically, the model group had pronounced lung injury, increased inflammatory cells and collagenous fibres and up‐regulated MMP9, TIMP‐1, INF‐<italic>γ</italic> and TGF‐<italic>β</italic> compared with control group. The histological appearance of lung inflammation and fibrosis and elevation of these parameters were inhibited in BMSCs treatment groups, among which, day 3 and day 6 treatment groups had less inflammatory cells and collagenous fibres than day 1 treatment group. BMSCs might suppress lung fibrosis and inflammation through down‐regulating MMP9, TIMP‐1, INF‐<italic>γ</italic> and TGF‐<italic>β</italic>. Delayed BMSCs treatment might exhibit a better therapeutic effect. Copyright © 2015 John Wiley & Sons, Ltd.</p> <p>Highlights are as follows: <list id="cbf3118-list-0001" list-type="order"><list-item id="cbf3118-li-0001"><p>BMSCs repair lung injury induced by BLM.</p></list-item><list-item id="cbf3118-li-0002"><p>BMSCs attenuate pulmonary fibrosis induced by BLM.</p></list-item><list-item id="cbf3118-li-0003"><p>BMSCs transplantation down‐regulates MMP9 and TIMP‐1.</p></list-item><list-item id="cbf3118-li-0004"><p>BMSCs transplantation down‐regulates INF‐<italic>γ</italic> and TGF‐<italic>β</italic>.</p></list-item><list-item id="cbf3118-li-0005"><p>Delayed transplantation timing of BMSCs might exhibit a better effect against BLM.</p></list-item></list></p> </abstract>