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Protection against hyperoxia‐induced lung fibrosis by KGF ‐induced MSC s mobilization in neonatal rats
Author(s) -
Yao Lan,
Liu Chengjun,
Luo Qing,
Gong Min,
Chen Jie,
Wang LiJia,
Huang Ying,
Jiang Xiaohua,
Xu Feng,
Li TingYu,
Shu Chang
Publication year - 2013
Publication title -
pediatric transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.457
H-Index - 69
eISSN - 1399-3046
pISSN - 1397-3142
DOI - 10.1111/petr.12133
Subject(s) - hyperoxia , medicine , keratinocyte growth factor , fibrosis , lung , pulmonary fibrosis , fibroblast growth factor , mediator , mobilization , cancer research , endocrinology , receptor , archaeology , history
MSC s have been shown to improve functional and pathological outcome in lung fibrosis. However, low in vivo cell engraftment of the transplanted cells limits their overall effectiveness. KGF (also known as FGF ‐7) is a critical mediator of pulmonary epithelial repair through stimulation of epithelial cell proliferation. However, the role of KGF in MSC s and its therapeutic effects have not been identified. In this study, we investigated the effect of KGF on MSC s and its preventive role in hyperoxia‐induced fibrosis in neonatal rats. Neonatal rats exposed to normoxia or hyperoxia were randomly assigned to receive intraperitoneal injections of normal saline ( PL ), MSC s, or KGF pretreated MSC s on the fourth day of exposure. Our results showed that as compared to PL , while MSC s attenuated lung fibrosis, KGF pretreated MSC s exhibited enhanced preventive effect against lung fibrosis. This effect was partly attributed to enhanced mobilization of MSC s to the fibrotic lungs. In addition, the SHH signaling pathway, which is associated with the differentiation of stem cells was activated by KGF . Our data suggest that MSC s, especially KGF preconditioned MSC s, can attenuate lung fibrosis and KGF may regulate the MSC s behavior by activating SHH pathway.