Publication: Microglia enhances proliferation of neural progenitor cells in an in vitro model of hypoxic-ischemic injury
Issued Date
2020-01-01
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ISSN
16112156
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2-s2.0-85090711419
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Mahidol University
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SCOPUS
Bibliographic Citation
EXCLI Journal. Vol.19, (2020), 950-961
Suggested Citation
Supanee Chounchay, Stephen C. Noctor, Nuanchan Chutabhakdikul Microglia enhances proliferation of neural progenitor cells in an in vitro model of hypoxic-ischemic injury. EXCLI Journal. Vol.19, (2020), 950-961. doi:10.17179/excli2020-2249 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/58924
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Title
Microglia enhances proliferation of neural progenitor cells in an in vitro model of hypoxic-ischemic injury
Abstract
© 2020, Leibniz Research Centre for Working Environment and Human Factors. All rights reserved. Microglial cells are the primary immune cells in the central nervous system. In the mature brain, microglia perform functions that include eliminating pathogens and clearing dead/dying cells and cellular debris through phagocyto-sis. In the immature brain, microglia perform functions that include synapse development and the regulation of cell production through extensive contact with and phagocytosis of neural progenitor cells (NPCs). However, the functional role of microglia in the proliferation and differentiation of NPCs under hypoxic-ischemic (HI) injury is not clear. Here, we tested the hypothesis that microglia enhance NPCs proliferation following HI insult. Primary NPCs cultures were divided into four treatment groups: 1) normoxic NPCs (NN); 2) normoxic NPCs cocultured with microglia (NN+M); 3) hypoxic NPCs (HN); and 4) hypoxic NPCs cocultured with microglia (HN+M). Hy-poxic-ischemic injury was induced by pretreatment of the cell cultures with 100 µM deferoxamine mesylate (DFO). NPCs treated with 100 µM DFO (HN groups) for 24 hours had significantly increased expression of hy-poxia-inducible factor 1 alpha (HIF-1α), a marker of hypoxic cells. Cell number, protein expression, mitosis, and cell cycle phase were examined, and the data were compared between the four groups. We found that the number of cells expressing the NPCs marker Sox2 increased significantly in the HN+M group and that the number of PH3-positive cells increased in the HN+M group; flow cytometry analysis showed a significant increase in the percentage of cells in the G2/M phase in the HN+M group. In summary, these results support the concept that microglia enhance the survival of NPCs under HI injury by increasing NPCs proliferation, survival, and differen-tiation. These results further suggest that microglia may induce neuroprotective effects after hypoxic injury that can be explored to develop novel therapeutic strategies for the treatment of HI injury in the immature brain.