Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

LRP5 and LRP6 are required for maintaining self-renewal and differentiation of hematopoietic stem cells

ABSTRACT: The canonical Wnt signaling pathway has been demonstrated as a critical role in the self-renewal, proliferation and differentiation of Hematopoietic Stem Cells (HSCs), but the functions are indeterminacy in adult HSCs since the different experimental systems using gain- or loss- functions mice models. Low-density lipoprotein receptor-related proteins 5 and 6 (LRP5 and LRP6) are important co-receptors in the canonical Wnt/β-catenin pathway. In this study, the knockout mice models were established for adult HSC investagation via conditional ablation of LRP5 and LRP6 in adult hematopoiesis by Vav-Cre Loxp system. We found the HSC numbers were diminished due to the decreased proliferation and cell cycle. To investigate the molecular mechanisms, RNA-seq was performed using HSC cells isolated from WT and dKO mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE122635 | GEO | 2018/12/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcriptome analysis of LRP5- and LRP6-depleted HCC38 cells.

Project description:In order to characterize the differences between the co-receptors LRP5 and LRP6, we have analyzed the transcriptome of HCC38 cells - a triple negative breast cancer cell line - 24, 48 and 72 hours following the depletion of LRP5 or LRP6 using siRNAs.

2018-06-06 | GSE109004 | GEO

Transcriptome analysis of Wnt3a-treated Wild Type, Lrp5KO , Lrp6KO and Lrp5/6KO osteoblasts

Project description:Wnt signaling is a major regulator of osteoblast differentiation and function. To investigate how Wnt3a signaling regulates osteoblastic gene expression and to identify the role of Lrp5 and Lrp6 in mediating Wnt3a signaling in osteoblasts, neonatal calvarial osteoblasts isolated from C57Bl6 (WT) and osteoblasts lacking Lrp5 (Lrp5KO), Lrp6 (Lrp6KO) and, both Lrp5 and 6 (Lrp5/6KO) were treated with Wnt3a for 24 hours and gene expression changes were quantified by RNA-seq.

2017-11-07 | GSE103492 | GEO

Transcriptome analysis of LRP5- and LRP6-depleted HCC38 cells.

Project description:Transcriptome analysis of LRP5- and LRP6-depleted HCC38 cells.

| PRJNA429432 | ENA

Proximity Labeling using Lrp6-Apex2 Identifies Multivesicular Endosomes and TFG as Modulators of Canonical Wnt Signaling

Project description:Proximity Labeling using Lrp6-Apex2 Identifies Multivesicular Endosomes and TFG as Modulators of Canonical Wnt Signaling

| MSV000084335 | MassIVE

Expression Analysis of Mammary Epithelial Cells Isolated from 12-16 Week Old Virgin C57Bl6 Lrp5+/+ and Lrp5-/- Mice

Project description:Investigation of whole-genome gene expression level changes in C57Bl6 Lrp5-/- mammary epithelial cells, compared to the wild-type strain. The mammary epithelial cells were isolated from numbers 4 and 5 mammary glands. The Lrp5-/- mouse strain described in this study has been further described in Lindvall C, Evans NC, Zylstra CR, Li Y, Alexander CM, Williams BO. 2006. The Wnt signaling receptor Lrp5 is required for mammary ductal stem cell activity and Wnt1-induced tumorigenesis. J Biol Chem. 2006 Nov 17;281(46):35081-7. Epub 2006 Sep 13. PMID: 16973609. Mammary epithelial cells were isolated from 6 groups of Lrp5+/+ and 3 groups of Lrp5-/- mice. The isolated RNA was submitted to the Gene Expression Center, University of Wisconsin-Madison where it was labelled with Cy3. Labelled samples were submitted to Roche Nimblegen and were hybridized to Mus musculus 1-Plex arrays that represent 42,586 mouse genes.

2010-05-19 | E-GEOD-19228 | biostudies-arrayexpress

The transcriptional response to Norrin/Fz4 signaling

Project description:Using mice with targeted gene mutations, we identify (1) distinct roles for different canonical Wnt signaling components in central nervous system (CNS) vascular development and in the specification of the blood-brain and blood-retina barriers (BBB and BRB) and (2) differential sensitivities of the vasculature in various CNS regions to perturbations in canonical Wnt signaling components. We find nearly equivalent roles for Lrp5 and Lrp6 in brain vascular development and barrier maintenance but a dominant role for Lrp5 in the retinal vasculature, an especially high sensitivity of the BBB in the cerebellum and pons/interpeduncular nuclei to decrements in canonical Wnt signaling, and plasticity in the barrier properties of mature CNS vasculature. Brain and retinal vascular defects caused by loss of Norrin/Frizzled4 signaling can be fully rescued by stabilizing beta-catenin, and loss of beta-catenin’s transcriptional activation domain or expression of a dominant negative Tcf4 recapitulates the vascular development and barrier defects seen with loss of receptor, co-receptor, or ligand, indicating that Norrin/Frizzled4 signaling acts predominantly by beta-catenin-dependent transcriptional regulation. This work strongly supports a model in which identical or nearly identical canonical Wnt signaling mechanisms mediate neural tube and retinal vascularization and maintain the BBB and BRB. Total retina RNA from P10 WT, NdpKO, Ctnnb1flex3/+;Pdgfb-CreER, and NdpKO;Ctnnb1flex3/+;Pdgfb-CreER mice was subjected to RNAseq

2014-06-05 | E-GEOD-56461 | biostudies-arrayexpress

Expression Analysis of Mammary Epithelial Cells Isolated from 12-16 Week Old Virgin C57Bl6 Lrp5+/+ and Lrp5-/- Mice

2009-12-01 | GSE19228 | GEO

Low-density lipoprotein receptor-5 contributes to whole body metabolism by regulating fatty acid metabolism in the osteoblast

Project description:Wnt signaling is critical for normal skeletal development as well as whole-body metabolic function. In this study, we described a previously unrecognized function for Wnt-Lrp5 signaling in the osteoblast that allows bone to acquire the resources necessary to fuel bone formation. Mice lacking the Lrp5 co-receptor specifically in osteoblasts and osteocytes exhibit the expected reductions in postnatal bone mass and also develop peripheral adiposity with corresponding reductions in energy expenditure. Conversely, mice expressing a high-bone mass mutant Lrp5 allele are leaner with reduced plasma triglyceride and free fatty acid levels. In this context, Wnt-initiated signals downstream of Lrp5, but not Lrp6, regulate the expression of key enzymes required for fatty acid β-oxidation. These results suggest that Wnt-Lrp5 signaling regulates basic cellular activities beyond those associated with fate-specification and differentiation in bone and that the skeleton influences global energy homeostasis via mechanisms independent of osteocalcin and glucose metabolism Total RNA isolated from cultures of Lrp5-deficient osteoblasts differentiated for 7 days in vitro compared to control osteoblasts

2014-03-14 | E-GEOD-55900 | biostudies-arrayexpress

LRP5 and LRP6 are required for maintaining self-renewal and differentiation of hematopoietic stem cells

Project description:LRP5 and LRP6 are required for maintaining self-renewal and differentiation of hematopoietic stem cells

| PRJNA505821 | ENA

Mitochondrial respiratory chain is essential for hematopoietic stem cell function

Project description:Adult and fetal hematopoietic stem cells (HSCs) display a glycolytic phenotype, which is required for maintenance of stemness; however, whether mitochondrial respiration is required to maintain HSC function is not known. Here we report that loss of the mitochondrial complex III subunit Rieske iron sulfur protein (RISP) in fetal mouse HSCs allows them to proliferate but impairs their differentiation, resulting in anemia and prenatal death. RISP null fetal HSCs displayed impaired respiration resulting in a decreased NAD+/NADH ratio. RISP null fetal HSCs and progenitors exhibited an increase in both DNA and histone methylation concomitant with increases in 2-hydroxyglutarate (2-HG), a metabolite known to inhibit DNA and histone demethylases. RISP inactivation in adult HSCs also impaired respiration resulting in loss of quiescence resulting in severe pancytopenia and lethality. Thus, respiration is dispensable for adult or fetal HSC proliferation, but essential for fetal HSC differentiation and maintenance of adult HSC quiescence.

2017-09-13 | PXD006054 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data