Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Comparison of gene expression profiles between a bone marrow-derived primary mesenchymal stromal cell clone (MSC2) without osteoblastic induction and with 14 days or 28 days of ostoblastic induction

ABSTRACT: Multiple hypothesis testing using a false discovery rate of p<0.01 and fold-change of 1.5 detected 4257 genes that were differentially expressed at least between two groups among MSC2 without osteoblastic induction, MSC2 with osteoblastic induction for 14 or 28 days

ORGANISM(S): Mus musculus

PROVIDER: GSE83770 | GEO | 2019/06/26

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Osteoblastic loss of Ezh2

Project description:Osteoblastic loss of Ezh2

| PRJNA436340 | ENA

Comparison of gene expression profiles between MC3T3-E1 without osteoblastic induction and with 14 days of ostoblastic induction

Project description:Microarray study revealed 1324 genes that were up-regulated and 1550 genes that were down-regulated more than 1.5 fold change (corrected p<0.05) in MC3T3-E1-derived-mature Osteoblasts compared to control MC3T3-E1.

2019-04-21 | GSE46400 | GEO

Osteoblastic response in human bone marrow stromal cells

2013-12-23 | GSE48907 | GEO

Mir-9-1 controls osteoblastic regulation of lymphopoiesis

Project description:The highly conserved MicroRNA-9 (miR-9) family consists of three members. We discovered that miR-9-1 deletion reduced mature miR-9 expression, causing 43% of the mice to display smaller size and postweaning lethality. MiR-9-1-deficient mice with growth defects experienced severe lymphopenia, but other blood cells were unaffected. The lymphopenia wasn’t due to defects in hematopoietic progenitors, as mutant bone marrow (BM) cells underwent normal lymphopoiesis after transplantation into wild-type recipients. Additionally, miR-9-1-deficient mice exhibited impaired osteoblastic bone formation, as mutant mesenchymal stem cells (MSCs) failed to differentiate into osteoblastic cells (OBs). RNA sequencing revealed reduced expression of master transcription factors for osteoblastic differentiation, Runt-related transcription factor 2 (Runx2) and Osterix (Osx), and genes related to collagen formation, extracellular matrix organization, and cell adhesion, in miR-9-1-deficient MSCs. Follistatin (Fst), an antagonist of bone morphogenetic proteins (BMPs), was found to be a direct target of miR-9-1. Its deficiency led to the up-regulation of Fst, inhibiting BMP signaling in MSCs, and reducing IL-7 and IGF-1. Thus, miR-9-1 controls osteoblastic regulation of lymphopoiesis by targeting the Fst/BMP/Smad signaling axis.

2023-08-31 | GSE239376 | GEO

Genomic characterization of osteoblastic differentiation of MC-3T3E1 cells

Project description:Gene expression analysis of murine MC3T3-E1 cells induced to undergo synchronized osteoblastic differentiation in vitro.

2012-06-28 | GSE30393 | GEO

Osteoblastic response in human bone marrow stromal cells

Project description:Our goal was to determine whether osteoblastic LuCaP 23.1 prostate cancer xenograft tumors can elicit an osteoblastic response at the gene expression level in human bone marrow stromal cells. Custom Agilent 44K whole human genome expression oligonucleotide microarrays were used to profile bone marrow stroma cells isolated from three patients and treated with either mineralization media or LuCaP 23.1 conditioned medium. Total RNA was isolated and amplified prior to hybridization against a common reference pool of prostate tumor cell lines.

2013-12-23 | E-GEOD-48907 | biostudies-arrayexpress

Effects of Hsd11b1 overexpressing in mc3T3-e1 pre-osteoblastic cell lines under glucocorticoid excess

Project description:To explore the mechanism by which osteoblastic 11β-HSD1 regulates bone formation and glucose handling, we transfected the mouse MC3T3-E1 osteoblastic cells with a plasmid carrying the exogenous Hsd11b1 or EGFP gene to construct the 11β-HSD1-overexpressed and control osteoblastic cells (hereafter MC3T3-HSD1 and MC3T3-GFP cells), respectively. After incubating with 11-DHC,we then employed RNA sequencing (RNA-seq) to examine the gene expression profile between MC3T3-HSD1 and MC3T3-GFP cells.

2024-09-25 | GSE274790 | GEO

Transcriptomic analyses of the anti-adipogenic and pro-osteoblastic effects of aspirin in rat bone mesenchymal stem cell

Project description:Theoretically, the differentiation of mesenchymal stem cells (MSCs) into either adipocytic or osteoblastic phenotype can be deemed as a seesaw, where induction of one lineage comes at the expense of the other. Previously, researchers, including our team, found that aspirin promoted osteoblast differentiation of bone mesenchymal stem cells (BMSCs) whereas inhibiting adipogenic differentiation. However, the precise mechanisms, that is, which pathways, what biological process or key genes involved during this process, had not been systematically studied. In the present study, we tend to analyze the whole transcriptome of the anti-adipogenic and promote-osteoblastic effects of aspirin in BMSCs. Our results showed that aspirin’s presence restored or further strengthened the expression of an important part of the gene population repressed during adipogenesis or increased during osteogenesis. Besides, classical pathways related to osteogenic differentiation (p53 signaling pathway, focal adhesion, osteoclast differentiation, PI3K-Akt signaling pathway, MAPK signaling pathway, and Wnt signaling pathway) and the fat metabolism were also disturbed during the promote-osteoblastic and anti-adipogenic effects of aspirin. Therefore, our whole-genome transcriptomic results shed new light and open the door to more specific “omics” studies. Our results allow a better understanding of the anti-adipogenic and promote-osteoblastic effects of aspirin and pave the way to aspirin clinical use for the prevention and treatment of diseases like tissue defect and osteoporosis.

2022-01-01 | GSE186026 | GEO

Effects of Hsd11b1 overexpressing in mc3T3-e1 pre-osteoblastic cell lines under glucocorticoid excess (ATAC-Seq)

Project description:To explore the mechanism by which osteoblastic 11β-HSD1 regulates bone formation and glucose handling, we transfected the mouse MC3T3-E1 osteoblastic cells with a plasmid carrying the exogenous Hsd11b1 or EGFP gene to construct the 11β-HSD1-overexpressed and control osteoblastic cells (hereafter MC3T3-HSD1 and MC3T3-GFP cells), respectively. After incubating with 11-DHC,we then employed assay for transposase-accessible chromatin with sequencing (ATAC-seq) to examine the gene expression profile between MC3T3-HSD1 and MC3T3-GFP cells.

2024-09-25 | GSE274974 | GEO

Ageing in space: microgravity triggers ferroptosis and accelerates senescence in osteoblastic cells

Project description:To understand the cellular and molecular mechanisms allowing MG63 osteoblastic cells to perceive, transduce and react to microgravity environment.

2023-12-20 | GSE224805 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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