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Endogenous beta-galactosidase activity marks TREM2-expressing Kupffer cell population in the livers of carbon tetrachloride-treated Lgr5-LacZ mice

ABSTRACT: Endogenous beta-galactosidase activity marks TREM2-expressing Kupffer cell population in the livers of carbon tetrachloride-treated Lgr5-LacZ mice

PROVIDER: PRJNA546516 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9202900.fastq.gz	Fastqsanger.gz
	SRR9202901.fastq.gz	Fastqsanger.gz
	SRR9202902.fastq.gz	Fastqsanger.gz
	SRR9202903.fastq.gz	Fastqsanger.gz
	SRR9202904.fastq.gz	Fastqsanger.gz

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Endogenous beta-galactosidase activity marks TREM2-expressing Kupffer cell population in the livers of carbon tetrachloride-treated Lgr5-LacZ mice

Project description:Lgr5+ cells isolated from liver organoids act as bipotent liver progenitors. Beta-galactosidase (beta-gal)-expressing cells appear in injured livers of Lgr5-LacZ mice, however, their origin and identity has remained controversial. Here we sought to clarify this issue. The majority of beta-gal+ cells emerged in pericentral regions of the liver lobule. Lineage tracing demonstrated that beta-gal+ cells did not originate from hepatocytes or cholangiocytes. Beta-gal+ cells were negative for hepatocyte and cholangiocyte markers; but positive for Kupffer cell markers. Transcriptome analysis revealed the expression of endogenous beta-galactosidase Glb1 and genes characteristic of TREM2+ macrophages that may regulate stem cell maintenance. We were not able to detect the expression of the Lgr5-LacZ transgene and concluded that the transgene was silenced.

2019-11-14 | GSE132206 | GEO

Resident Kupffer cell maladaptation in Liver Fibrosis is Rescued by Monocyte-Derived Syncytia of Macrophages

Project description:To investigate the effects of liver fobrosis and alteration in liver architecture in the regulation of embryonic Kupffer cells identity and funtion, we used a well stablished carbon tetrachloride model to induce liver fibrosis.

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Comparison of two A. nidulans strains: control CV125 and transgenic NA1363 harboring E. coli LacZ transgene.

Project description:Transcriptional profiling of two A. nidulans strains, aiming to compare the control strain CV125 (pabaA1) with the transgenic strain NA1363 (pabaA1) harbouring a gpdAp-lacZ-trpCt.riboB construct integrated in chromosome VIII. This construct, carried out in a derivative of the pBR322 vector, contained the E. coli lacZ sequence (encoding ß-galactosidase) fused to the A. nidulans trpC terminator and placed under the control of the strong and constitutive promoter of the A. nidulans gpdA gene, and the riboB gene as a selection marker.

2016-04-12 | GSE76918 | GEO

In vitro expansion of single adult Lgr5+ liver cells induced by Wnt-driven regeneration

Project description:The Wnt target gene Lgr5 marks actively dividing stem cells in Wnt-driven, self-renewing tissues such as small intestine and colon, stomach and hair follicles. A 3D culture system allows long-term clonal expansion of single Lgr5+ stem cells into transplantable organoids that retain many characteristics of the original epithelial architecture. A crucial component of the culture medium is the Wnt agonist Rspo, the recently discovered ligand of Lgr5. Here we show that Lgr5-LacZ is not expressed in healthy adult liver, yet that small Lgr5-LacZ+ cells appear near bile ducts upon damage, coinciding with robust activation of Wnt signaling. As shown by lineage tracing using a novel Lgr5-ires-CreERT2 knock-in allele, damage-induced Lgr5+ cells generate hepatocytes and bile ducts in vivo. Single Lgr5+ cells from damaged liver can be clonally expanded as organoids in Rspo1-based culture medium over multiple months. Such clonal organoids can be induced to differentiate in vitro and to generate functional hepatocytes upon transplantation into FAH-/- mice. These findings imply that previous findings on Lgr5+ stem cells in actively self-renewing tissues extend to damage-induced stem cells in a tissue with a low rate of spontaneous self-renewal.

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Project description:The molecular mechanisms controlling stem cell renewal and lineage commitment are still poorly understood due to lack of reliable markers. In the adult small intestine, an example of high rate self-renewing tissue, four different epithelial cell lineages (enterocytes, Goblet, enteroendocrine and Paneth cells) are generated from a pool of stem cells localised at the bottom of the crypts of Lieberkühn. Recently, the orphan Leucine-rich repeat G protein-coupled receptor 5 (GPR49), a target of Wnt signalling, has been proposed as a marker for such cells. We investigated the role of LGR5 during intestinal development by using LGR5 null/LacZ-NeoR knock-in mice. We show that LGR5 deficiency leads to premature Paneth cell differentiation. X-gal staining on E18.5 intestine revealed that LGR5 expression is restricted to a few cells clustered within the intervillus region known to contain progenitor cells. In LGR5-null mice, expression from the LGR5 promoter was found upregulated, suggesting a loss of negative feedback control. However, neither epithelial cell proliferation nor cell migration appeared significantly impaired by LGR5 deficiency. Finally, transcriptional profiling of ileal mutant mice suggests that LGR5 plays a role in regulating the Wnt and Notch signalling pathways controlling progenitor renewal and differentiation.

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Carbon tetrachloride (CCl4) induced liver fibrosis

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Transcription profiling of spinal cord from Math1-LacZ/+ and Math1-LacZ/- E12.5 mice

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2008-03-13 | E-MEXP-1492 | biostudies-arrayexpress

Carbon tetrachloride and Acetaminophen hepatotoxicity study

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2007-02-27 | GSE4874 | GEO

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