Peptide KLF14-P1 secreted from mesenchymal stem cells protects against
bronchopulmonary dysplasia both in vivo and in vitro
Abstract
Background: Mesenchymal stem cells (MSCs) have been confirmed to harbor
therapeutic potential in bronchopulmonary dysplasia (BPD). Nevertheless,
the possible influence of peptides secreted from MSCs remains clarified.
Herein, this study focused on investigating the potential role of
peptide KLF14-P1 (271TKHARRHP278, Named after the precursor protein
Krueppel-like factor 14, KLF14) secreted from MSCs in BPD both in vivo
and in vitro. Methods: Firstly, the mouse BPD model was constructed, and
administrated with KLF14-P1 (10, 50 and 100 μg/g). General basic
characteristics were observed. Pathological change of lung tissues was
determined by HE analysis. Besides, the number and proportion of cells
in broncho alveolar lavage fluid (BALF) were analyzed. The inflammatory
factor (IL-1β, IL-6, TNF-α and IL-10) expressions in BALF and lung
tissues were analyzed through ELISA, QRT-PCR and western blot. Moreover,
MLE-12 cells stimulated with H2O2 (1 mM) was adopted construct in vitro
BPD model. CCK-8, qRT-PCR, western blot and ELISA were carried out to
evaluate the effects of KLF14-P1 (10, 50 and 100 μM) on H2O2-treated
MLE-12 cell proliferation and inflammatory responses. The role of
KLF14-P1 in the oxidative stress was evaluated by analysis. Results: In
vivo, KLF14-P1 improved BPD mice accompanied with decreasing
inflammatory infiltration and reducing lung dry / wet weight ratio.
Moreover, in vitro, CCK-8 revealed that KLF14-P1 improved the viability
MLE-12 cells treated with H2O2. In addition, KLF14-P1 notably inhibited
the apoptosis of H2O2-treated MLE-12 cells. Besides, KLF14-P1 obviously
ameliorated inflammatory responses of H2O2-treated MLE-12 cells.
Conclusion: KLF14-P1 exhibited potential therapeutic properties against
BPD.