Project description:The winged helix transcription factor Foxl1 is a marker for progenitor cells and their descendants in the mouse liver in vivo. Here, we purify progenitor cells from Foxl1-Cre; RosaYFP mice and evaluate their proliferative and differentiation potential in vitro. Treatment of Foxl1-Cre; RosaYFP mice with 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet led to an increase of the percentage of YFP-labeled Foxl1+ cells. Clonogenic assays demonstrated that up to 3.6% of Foxl1+ cells had proliferative potential. Foxl1+ cells differentiated into cholangiocytes and into hepatocytes in vitro, depending on the culture condition employed. Microarray analyses indicated that Foxl1+ cells express stem cell markers such as Prom1 as well as differentiation markers such as Ck19 and Hnf4a. Thus, the Foxl1-Cre; RosaYFP model allows for easy isolation of adult hepatic progenitor cells that can be expanded and differentiated in culture. Refer to individual Series. This SuperSeries is composed of the following subset Series: GSE28890: Foxl1-Cre-marked Adult Hepatic Progenitors Have Clonogenic and Bi-Lineage Differentiation Potential - Time Course GSE28891: Foxl1-Cre-marked Adult Hepatic Progenitors Have Clonogenic and Bi-Lineage Differentiation Potential - Differentiated vs Primary
Project description:The winged helix transcription factor Foxl1 is a marker for progenitor cells and their descendants in the mouse liver in vivo. Here, we purify progenitor cells from Foxl1-Cre; RosaYFP mice and evaluate their proliferative and differentiation potential in vitro. Treatment of Foxl1-Cre; RosaYFP mice with 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet led to an increase of the percentage of YFP-labeled Foxl1+ cells. Clonogenic assays demonstrated that up to 3.6% of Foxl1+ cells had proliferative potential. Foxl1+ cells differentiated into cholangiocytes and into hepatocytes in vitro, depending on the culture condition employed. Microarray analyses indicated that Foxl1+ cells express stem cell markers such as Prom1 as well as differentiation markers such as Ck19 and Hnf4a. Thus, the Foxl1-Cre; RosaYFP model allows for easy isolation of adult hepatic progenitor cells that can be expanded and differentiated in culture. In vitro Differentiated cells were compared to Primary cells
Project description:The winged helix transcription factor Foxl1 is a marker for progenitor cells and their descendants in the mouse liver in vivo. Here, we purify progenitor cells from Foxl1-Cre; RosaYFP mice and evaluate their proliferative and differentiation potential in vitro. Treatment of Foxl1-Cre; RosaYFP mice with 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet led to an increase of the percentage of YFP-labeled Foxl1+ cells. Clonogenic assays demonstrated that up to 3.6% of Foxl1+ cells had proliferative potential. Foxl1+ cells differentiated into cholangiocytes and into hepatocytes in vitro, depending on the culture condition employed. Microarray analyses indicated that Foxl1+ cells express stem cell markers such as Prom1 as well as differentiation markers such as Ck19 and Hnf4a. Thus, the Foxl1-Cre; RosaYFP model allows for easy isolation of adult hepatic progenitor cells that can be expanded and differentiated in culture.
Project description:The winged helix transcription factor Foxl1 is a marker for progenitor cells and their descendants in the mouse liver in vivo. Here, we purify progenitor cells from Foxl1-Cre; RosaYFP mice and evaluate their proliferative and differentiation potential in vitro. Treatment of Foxl1-Cre; RosaYFP mice with 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet led to an increase of the percentage of YFP-labeled Foxl1+ cells. Clonogenic assays demonstrated that up to 3.6% of Foxl1+ cells had proliferative potential. Foxl1+ cells differentiated into cholangiocytes and into hepatocytes in vitro, depending on the culture condition employed. Microarray analyses indicated that Foxl1+ cells express stem cell markers such as Prom1 as well as differentiation markers such as Ck19 and Hnf4a. Thus, the Foxl1-Cre; RosaYFP model allows for easy isolation of adult hepatic progenitor cells that can be expanded and differentiated in culture.
Project description:The winged helix transcription factor Foxl1 is a marker for progenitor cells and their descendants in the mouse liver in vivo. Here, we purify progenitor cells from Foxl1-Cre; RosaYFP mice and evaluate their proliferative and differentiation potential in vitro. Treatment of Foxl1-Cre; RosaYFP mice with 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet led to an increase of the percentage of YFP-labeled Foxl1+ cells. Clonogenic assays demonstrated that up to 3.6% of Foxl1+ cells had proliferative potential. Foxl1+ cells differentiated into cholangiocytes and into hepatocytes in vitro, depending on the culture condition employed. Microarray analyses indicated that Foxl1+ cells express stem cell markers such as Prom1 as well as differentiation markers such as Ck19 and Hnf4a. Thus, the Foxl1-Cre; RosaYFP model allows for easy isolation of adult hepatic progenitor cells that can be expanded and differentiated in culture. This SuperSeries is composed of the SubSeries listed below.
Project description:The winged helix transcription factor Foxl1 is a marker for progenitor cells and their descendants in the mouse liver in vivo. Here, we purify progenitor cells from Foxl1-Cre; RosaYFP mice and evaluate their proliferative and differentiation potential in vitro. Treatment of Foxl1-Cre; RosaYFP mice with 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet led to an increase of the percentage of YFP-labeled Foxl1+ cells. Clonogenic assays demonstrated that up to 3.6% of Foxl1+ cells had proliferative potential. Foxl1+ cells differentiated into cholangiocytes and into hepatocytes in vitro, depending on the culture condition employed. Microarray analyses indicated that Foxl1+ cells express stem cell markers such as Prom1 as well as differentiation markers such as Ck19 and Hnf4a. Thus, the Foxl1-Cre; RosaYFP model allows for easy isolation of adult hepatic progenitor cells that can be expanded and differentiated in culture. There were 26 samples used in the analysis. Typically 4 replicates for each of 7 conditions, except for two condtions which had only 3 replicates. Day 0 samples are non-parenchymal cells without DDC treatment. YFP_pos samples are YFP-expressing non-parenchymal cells induced by Foxl1-CRE after 3, 7 or 14 days of DDC treatment. YFP_neg samples are analogous but do not expressed YFP.
Project description:We found that hepatic injury induced by PTEN loss establishes a selection pressure for tumorinitiating cells (TICs) to proliferate and form mixed lineage tumors. The Pten null mice demonstrate escalating levels of hepatic injury prior to proliferation of hepatic progenitors. Attenuation of hepatic injury by deleting Akt2 reduces progenitor cell proliferation and delays tumor development. Treatment of double mutant mice with 3,5-dietoxycarbonyl-1,4 dihydrocollidine (DDC) shows that the primary effect of AKT2 loss is attenuation of hepatic injury and not inhibition of progenitor cell proliferation in response to injury. Pten/Akt2 double mutant (PtenloxP/loxP; Akt2-/-; Alb-Cre+) (Dm) were generated by crossing the PtenloxP/loxP; Alb-Cre+ (Pm) with the Akt2-/- mice [19]. Control animals are PtenloxP/loxP; Albumin (Alb)-Cre-.
Project description:Acute erythroid leukemia (AEL) most commonly involves transformation of both the myeloid and erythroid lineages. However, the mutations that cause AEL and the nature of the transformed cell that sustains the bi-lineage leukemia phenotype remain unknown. We here show that combined bi-alleCD45.2+LKFcgRII/III+CD55- C/EBPa and GATA-2 zinc finger 1 (ZnF1) mutations are sufficient to induce bi-lineage AEL, and that the leukemia-initiating cell has a Lin–Sca-1–c-Kit+CD150–FcyRII/III+ surface phenotype, consistent with a committed myeloid progenitor. However, we find that in the presence of bi-alleCD45.2+LKFcgRII/III+CD55- C/EBPa mutation this cell population acquires ectopic erythroid gene expression and lineage potential, leading to the formation of neomorphic neutrophil-erythroid lineage progenitors, which upon transformation generate the bi-lineage leukemia-initiating cell. These results identify C/EBPa and GATA-2 ZnF1 mutations as causative of AEL, and demonstrate that transcriptional reprogramming by a leukemia-initiating mutation can re-define the lineage output of the resulting leukemia-initiating cells