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Article Abstract

Background: Pulmonary fibrosis is a pathological hallmark of lung injury. It is an aggressive disease that replaces normal lung parenchyma by fibrotic tissue. The transforming growth factor-beta-mothers against decapentaplegic homolog 3 (TGF-β1-Smad3) signaling pathway plays a key role in regulating lung fibrosis. (), a small leucine-rich proteoglycan, has a modulatory effect on the immune system by reversibly binding with TGF-β and reducing its bioavailability. Mesenchymal stem cell (MSC) therapy is a new strategy that has an immune-modulatory capacity.

Objective: The aim of this study was to introduce a new therapeutic approach to harness remodeling in injured lung.

Material And Methods: Bone marrow MSCs were isolated and transduced by gene. Lung injury was induced by bleomycin and mice were treated with MSCs, MSCs-, and . Then, oxidative stress biomarkers, remodeling biomarkers, bronchoalveolar lavage cells, and histopathology study were conducted.

Results: Reduced catalase and superoxide dismutase increased due to treatments. Elevated malondialdehyde, hydroxyproline, TGF-β levels, and polymorphonuclear cells count decreased in the treated groups. Additionally, the histopathology of lung tissues showed controlled inflammation and fibrosis.

Conclusion: Transfected gene to MSCs and used cell therapy could control remodeling and bleomycin-induced lung injury.

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Source
http://dx.doi.org/10.15586/aei.v52i4.1104DOI Listing

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