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EPO enhances the protective effects of MSCs in experimental hyperoxia-induced neonatal mice by promoting angiogenesis.
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- Additional Information
- Source:
Publisher: Impact Journals, LLC Country of Publication: United States NLM ID: 101508617 Publication Model: Print Cited Medium: Internet ISSN: 1945-4589 (Electronic) Linking ISSN: 19454589 NLM ISO Abbreviation: Aging (Albany NY) Subsets: MEDLINE
- Publication Information:
Original Publication: Albany, NY : Impact Journals, LLC
- Subject Terms:
- 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.
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- Contributed Indexing:
Keywords: BPD; EPO; MSCs; SDF-1/CXCR4; angiogenesis
- Accession Number:
0 (CXCR4 protein, mouse)
0 (Chemokine CXCL12)
0 (Receptors, CXCR4)
0 (Vascular Endothelial Growth Factor A)
11096-26-7 (Erythropoietin)
- Publication Date:
Date Created: 20190430 Date Completed: 20200521 Latest Revision: 20200521
- Publication Date:
20250114
- Accession Number:
PMC6519997
- Accession Number:
10.18632/aging.101937
- Accession Number:
31035257
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