Peptide KLF14-P1 secreted from mesenchymal stem cells protects against bronchopulmonary dysplasia both in vivo and in vitro

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.