Open Access

ARTICLE

Different sources of MSCs on pulmonary fibrosis in C57BL/6 mice

by Shucai Wu^1,#, Dengrui Li^1,#, Sumin Guo¹, Li Gao², Yonghui Yang^1,*

1 The Center of Lung Cancer Prevention, Hebei Province Chest Hospital, Shijiazhuang, 050041, China
2 College of Life Science, Hebei Normal University, Shijiazhuang, 050024, China

* Address correspondence to: Yonghui Yang,
# These authors contributed equally to this work

BIOCELL 2021, 45(2), 339-344. https://doi.org/10.32604/biocell.2021.011379

Received 04 May 2020; Accepted 07 October 2020; Issue published 19 February 2021

Abstract

Since stem cell therapy is the most effective treatment in the field of tissue reparation and reconstitution, the present study aimed to explore the different sources of mesenchymal stem cells (MSCs) on the different effects of pulmonary fibrosis-related cytokines in C57BL/6 mice. For reaching this goal, we isolated MSCs from umbilical cord blood and placenta and used for stem cell therapy in a mouse model of pulmonary fibrosis model. The pulmonary fibrosis model was done by injecting bleomycin into the trachea of C57BL/6 mice. Then we assessed the degree of pulmonary fibrosis in each mouse lung tissue at weeks 1, 2, 3, and 4. In addition, flow cytometry was used to evaluate the frequency of CD73, CD90, CD106, CD34, CD45, CD14 cells at the mononuclear cell level; and western blotting assays revealed the expression of IκB-α. Our results showed that stem cell therapy by placenta-derived MSC had a lower level of CD34, CD45, CD14 cells at the mononuclear cell level, and that improved pulmonary fibrosis at both molecular and pathological levels. In addition, western blotting assays revealed that the expression of IκB-α was down-regulated in MSC-treated animals. In addition, placenta-derived MSC was the most effective in improving pulmonary fibrosis in comparison to other sources. This study suggests that MSC might be a novel therapeutic approach in pulmonary fibrosis due to an enhanced anti-inflammatory effect. Also, MSC modification by gene editing could enhance their therapeutic effect in mouse pulmonary fibrosis.

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