Endogenous beta-galactosidase activity marks a TREM2-expressing Kupffer cell population in injured livers of Lgr5-LacZ and wild-type mice.
Mariliis KlaasKristina Mäemets-AllasKadi LõhmussaarMikk ToomingJaneli ViilViljar JaksPublished in: FEBS letters (2019)
Lgr5-LacZ mice harbor the Escherichia coli LacZ gene encoding β-galactosidase (β-gal) under the control of the Lgr5 promoter, a stem/progenitor cell marker. In injured livers of Lgr5-LacZ mice, cells expressing β-galactosidase (β-gal) are considered as potential bipotent liver progenitors; however, their origin and identity remain unknown. Unexpectedly, using lineage tracing, we demonstrate that the β-gal+ cells do not originate from liver parenchymal cells. Instead, β-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 β-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 β-gal expression is very low, suggesting transgene silencing. The gene expression profile of the β-gal+ Kupffer cells from injured livers suggests a role in liver regeneration.
Keyphrases
- induced apoptosis
- wild type
- cell cycle arrest
- escherichia coli
- poor prognosis
- endoplasmic reticulum stress
- metabolic syndrome
- stem cells
- gene expression
- type diabetes
- risk assessment
- high fat diet induced
- dna methylation
- oxidative stress
- transcription factor
- binding protein
- adipose tissue
- genome wide
- bone marrow
- pseudomonas aeruginosa
- staphylococcus aureus