| First Author | Chen HR | Year | 2020 |
| Journal | Sci Adv | Volume | 6 |
| Issue | 35 | Pages | eabb2119 |
| PubMed ID | 32923636 | Mgi Jnum | J:314192 |
| Mgi Id | MGI:6790752 | Doi | 10.1126/sciadv.abb2119 |
| Citation | Chen HR, et al. (2020) Fate mapping via CCR2-CreER mice reveals monocyte-to-microglia transition in development and neonatal stroke. Sci Adv 6(35):eabb2119 |
| abstractText | Whether monocytes contribute to the brain microglial pool in development or after brain injury remains contentious. To address this issue, we generated CCR2-CreER mice to track monocyte derivatives in a tamoxifen-inducible manner. This method labeled Ly6C(hi) and Ly6C(lo) monocytes after tamoxifen dosing and detected a surge of perivascular macrophages before blood-brain barrier breakdown in adult stroke. When dosed by tamoxifen at embryonic day 17 (E17), this method captured fetal hematopoietic cells at E18, subdural Ki67(+) ameboid cells at postnatal day 2 (P2), and perivascular microglia, leptomeningeal macrophages, and Iba1(+)Tmem119(+)P2RY12(+) parenchymal microglia in selective brain regions at P24. Furthermore, this fate mapping strategy revealed an acute influx of monocytes after neonatal stroke, which gradually transformed into a ramified morphology and expressed microglial marker genes (Sall1, Tmem119, and P2RY12) for at least 62 days after injury. These results suggest an underappreciated level of monocyte-to-microglia transition in development and after neonatal stroke. |
