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Research Paper|Volume 11, Issue 8|pp 2477—2487

EPO enhances the protective effects of MSCs in experimental hyperoxia-induced neonatal mice by promoting angiogenesis

Chao Sun1, Shanshan Zhang2, Jue Wang1, Wen Jiang1, Qian Xin1, Xiaojing Chen1, Zhaohua Zhang3, Yun Luan1
  • 1Central Research Laboratory, The Second Hospital of Shandong University, Jinan 250033, PR China
  • 2Department of Emergency, The Second Hospital of Shandong University, Jinan 250033, PR China
  • 3Department of Pediatrics, The Second Hospital of Shandong University, Jinan 250033, PR China

* * Equal contribution

Received: March 6, 2019Accepted: April 24, 2019Published: April 29, 2019
https://doi.org/10.18632/aging.101937

Copyright: Sun et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Bronchopulmonary dysplasia (BPD) is the most common type of chronic lung disease in infancy; however, there is no effective treatment for it. In the present study, a neonatal mouse BPD model was established by continuous exposure to high oxygen (HO) levels. Mice were divided randomly into 5 groups: control, BPD, EPO, MSCs, and MSCs+EPO. At 2 weeks post-treatment, vessel density and the expression levels of endothelial growth factor (VEGF), stromal cell-derived factor-1 (SDF-1), and its receptor C-X-C chemokine receptor type 4 (CXCR4) were significantly increased in the MSC+EPO group compared with the EPO or MSCs group alone; moreover, EPO significantly enhanced MSCs proliferation, migration, and anti-apoptosis ability in vitro. Furthermore, the MSCs could differentiate into cells that were positive for the type II alveolar epithelial cell (AECII)-specific marker surfactant protein-C, but not positive for the AECI-specific marker aquaporin 5. Our present results suggested that MSCs in combination with EPO could significantly attenuate lung injury in a neonatal mouse model of BPD. The mechanism may be by the indirect promotion of angiogenesis, which may involve the SDF-1/CXCR4 axis.