A Novel Endogenous Damage Signal, CSF-2, Activates Multiple Beneficial Functions of Adipose Tissue-Derived Mesenchymal Stem Cells
- Authors
- Park, Se-Ra; Cho, Ara; Kim, Jae-Wan; Lee, Hwa-Yong; Hong, In-Sun
- Issue Date
- 5-Jun-2019
- Publisher
- CELL PRESS
- Keywords
- Akt; CSF-2; differentiation; ERK1/2; growth; migration; MSCs; stemness
- Citation
- MOLECULAR THERAPY, v.27, no.6, pp.1087 - 1100
- Journal Title
- MOLECULAR THERAPY
- Volume
- 27
- Number
- 6
- Start Page
- 1087
- End Page
- 1100
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/1341
- DOI
- 10.1016/j.ymthe.2019.03.010
- ISSN
- 1525-0016
- Abstract
- The major challenges of current mesenchymal stem cell (MSC)-based therapeutics are their low differentiation potential into specialized cell types and their homing ability to sites of injury. Therefore, many researchers have directed their efforts toward finding a novel stimulatory factor that can significantly enhance the therapeutic effects of MSCs. Colony-stimulating factor 2 (CSF-2) is previously known as a hematopoietic growth factor involved in the differentiation of various myeloid cells from hematopoietic progenitor cells. In addition to this canonical hematopoietic function, we identified for the first time that CSF-2 is actively secreted by stem cells, in response to various types of injuries, as an endogenous damage signal that promotes the therapeutic effects of MSCs by enhancing their multi-lineage differentiation and migratory capacities, possibly through its receptor CD116. Our results also revealed that CSF-2 exerts its stimulatory effects on MSCs via PI3K/Akt-and/or FAK/ERK1/2-signaling pathways. More importantly, we also found that MSCs stimulated with CSF-2 show markedly enhanced differentiation and migratory capacities and subsequent in vivo therapeutic effects in an endometrial ablation animal model. Collectively, our findings provide compelling evidence for a novel non-hematopoietic function of CSF-2 in promoting multiple beneficial functions of MSCs via a non-canonical mechanism as an endogenous damage signal.
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