| First Author | Klaas M | Year | 2020 |
| Journal | FEBS Lett | Volume | 594 |
| Issue | 5 | Pages | 958-970 |
| PubMed ID | 31705801 | Mgi Jnum | J:339737 |
| Mgi Id | MGI:6441659 | Doi | 10.1002/1873-3468.13669 |
| Citation | Klaas M, et al. (2020) Endogenous beta-galactosidase activity marks a TREM2-expressing Kupffer cell population in injured livers of Lgr5-LacZ and wild-type mice. FEBS Lett 594(5):958-970 |
| abstractText | Lgr5-LacZ mice harbor the Escherichia coli LacZ gene encoding beta-galactosidase (beta-gal) under the control of the Lgr5 promoter, a stem/progenitor cell marker. In injured livers of Lgr5-LacZ mice, cells expressing beta-galactosidase (beta-gal) are considered as potential bipotent liver progenitors; however, their origin and identity remain unknown. Unexpectedly, using lineage tracing, we demonstrate that the beta-gal(+) cells do not originate from liver parenchymal cells. Instead, beta-gal(+) cells, isolated from injured livers of both Lgr5-LacZ and wild-type mice, are positive for markers of Kupffer cells, liver-resident macrophages. The beta-gal expression in these cells is a result of elevated expression of the endogenous beta-galactosidase Glb1. In injured livers of Lgr5-LacZ mice, bacterial beta-gal expression is very low, suggesting transgene silencing. The gene expression profile of the beta-gal(+) Kupffer cells from injured livers suggests a role in liver regeneration. |
