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Ubiquitin-specific protease USP34 controls osteogenic differentiation and bone formation by regulating BMP2 signaling

ABSTRACT: Ubiquitin-specific protease USP34 controls osteogenic differentiation and bone formation by regulating BMP2 signaling

PROVIDER: PRJNA476060 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7340400.fastq.gz	Fastqsanger.gz
	SRR7340401.fastq.gz	Fastqsanger.gz
	SRR7340402.fastq.gz	Fastqsanger.gz
	SRR7340399.fastq.gz	Fastqsanger.gz

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Ubiquitin-specific protease USP34 controls osteogenic differentiation and bone formation by regulating BMP2 signaling.

Project description:The osteogenic differentiation of mesenchymal stem cells (MSCs) is governed by multiple mechanisms. Growing evidence indicates that ubiquitin-dependent protein degradation is critical for the differentiation of MSCs and bone formation; however, the function of ubiquitin-specific proteases, the largest subfamily of deubiquitylases, remains unclear. Here, we identify USP34 as a previously unknown regulator of osteogenesis. The expression of USP34 in human MSCs increases after osteogenic induction while depletion of USP34 inhibits osteogenic differentiation. Conditional knockout of Usp34 from MSCs or pre-osteoblasts leads to low bone mass in mice. Deletion of Usp34 also blunts BMP2-induced responses and impairs bone regeneration. Mechanically, we demonstrate that USP34 stabilizes both Smad1 and RUNX2 and that depletion of Smurf1 restores the osteogenic potential of Usp34-deficient MSCs in vitro Taken together, our data indicate that USP34 is required for osteogenic differentiation and bone formation.

| S-EPMC6187217 | biostudies-literature

Ubiquitin-specific protease USP34 controls osteogenic differentiation and bone formation by regulating BMP2 signaling.

Project description: Not available

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Ubiquitin-specific protease USP34 controls osteogenic differentiation and bone formation by regulating BMP2 signaling

Project description:The aim is to analyze the transcriptome profiling (RNA-seq) of Mettl3 knockout mesenchymal stem cells (MSCs) and identify m6A modified mRNThe aim is to analyze the transcriptome profiling (RNA-seq) of USP34 knockdown mesenchymal stem cells (MSCs). Total RNAs from human MSCs of siCTRL and siUSP34 were extracted using an RNeasy mini kit (Qiagen). Libraries were prepared using the Illumina TrueSeq mRNA sample preparation kit according to manufacturer’s instruction, and single-end sequenced on an Illumina HiSeq 3000 machine. The reads were aligned to hg19 genome using Tophat. Analysis of RNA-seq data was done using Cufflinks with Refseq mRNAs to guide assembly and the cummeRbund package in R. Transcripts, which were regulated greater than 2-fold were considered significant difference.

2018-09-01 | GSE115789 | GEO

BMP2 and GSK126 synergize to induce expression of osteogenic genes

Project description:BMP2 and GSK126 synergize to induce expression of osteogenic genes

2019-12-01 | GSE135984 | GEO

Effect of Mirn378 overexpression on gene expression during C2C12 myogenic and BMP2-induced osteogenic differentiation

2014-01-28 | GSE51883 | GEO

Effect of Mirn378 overexpression on gene expression during C2C12 myogenic and BMP2-induced osteogenic differentiation

Project description:Background: MicroRNAs (miRNAs) are a family of small, non-coding single-stranded RNA molecules involved in post-transcriptional regulation of gene expression. As such, they are believed to play a role in regulating the step-wise changes in gene expression patterns that occur during cell fate specification of multipotent stem cells. Here, we have studied whether terminal differentiation of C2C12 myoblasts is indeed controlled by lineage-specific changes in miRNA expression. Results: Using a previously generated RNA polymerase II (Pol-II) ChIP-on-chip dataset, we show differential Pol-II occupancy at the promoter regions of six miRNAs during C2C12 myogenic versus BMP2-induced osteogenic differentiation. Overexpression of one of these miRNAs, miR-378, enhances Alp activity, calcium deposition and mRNA expression of osteogenic marker genes in the presence of BMP2. Conclusions: Our results demonstrate a previously unknown role for miR-378 in promoting BMP2-induced osteogenic differentiation. Stable C2C12 cell lines C2C12-pMirn0 and C2C12-pMirn378 were generated by lentiviral transduction of C2C12 myoblasts with a Mirn378-overexpression construct and its parent vector, respectively. C2C12-pMirn0 and C2C12-pMirn378 cells were plated at 2.5 x 10^4 cells/cm2 (day -1), cultured for 1 day in DMEM 10%NCS, then (d0) treated with or without 300 ng/ml bone morphogenetic protein 2 (BMP2) for 6 days. RNA was extracted on d0, d3 and d6 and hybridized to GeneChip Mouse Genome 430 2.0 array (Affymetrix).

2014-01-28 | E-GEOD-51883 | biostudies-arrayexpress

BMP2 and GSK126 synergize to induce expression of osteogenic genes

Project description:BMP2 and GSK126 synergize to induce expression of osteogenic genes

| PRJNA560888 | ENA

USP34 controls osteogenic differentiation and bone formation by regulating BMP2 signaling

Project description:The osteogenic differentiation of mesenchymal stem cells (MSCs) is governed by multiple mechanisms. Growing evidence indicates that ubiquitin-dependent protein degradation is critical for the differentiation of MSCs and bone formation; however, the function of ubiquitin-specific proteases, the largest subfamily of deubiquitylases, remains unclear. Here we identify USP34 as a previously unknown regulator of osteogenesis. The expression of USP34 in human MSCs increases after osteogenic induction while depletion of USP34 inhibits osteogenic differentiation. Conditional knockout of Usp34 from MSCs or pre-osteoblasts leads to low bone mass in mice. Deletion of Usp34 also blunts BMP2-induced responses and impairs bone regeneration. Mechanically, we demonstrate that USP34 stabilizes both Smad1 and RUNX2 and that depletion of Smurf1 restores the osteogenic potential of Usp34-deficient MSCs in vitro. Taken together, our data indicate that USP34 is required for osteogenic differentiation and bone formation.

| S-SCDT-EMBOJ-2018-99398 | biostudies-other

Mouse primary osteoblasts treated with/without BMP2

Project description:Bone morphogenetic proteins (BMPs) regulate many aspects of skeletal development, including osteoblast and chondrocyte differentiation, cartilage and bone formation, and cranial and limb development. Among them, BMP2, one of the most potent osteogenic signaling molecules, stimulates osteoblast differentiation.

2012-03-30 | GSE36925 | GEO

Bone morphogenetic protein-2 (BMP2) and estradiol-17β (E2)-induced changes in ovarian transcriptome during primordial follicle formation in the mouse ovary

Project description:Estradiol-17β (E2) has been shown to promote primordial follicle (PF) formation and to involve BMP2 as a downstream effector to promote PF in the hamsters. However, the molecular mechanism whereby these factors regulate ovarian somatic cells to pre-granulosa cells (preGC) transition leading to PF formation remains unclear. The objective of this study was to determine whether BMP2 and/or E2 would regulate the expression of specific ovarian transcriptome during preGC transition and PF formation in the mouse ovary. BMP2 mRNA level increased during the period of PF formation with concurrent presence of BMP2 protein in ovarian somatic cells. E2 but not BMP2 exposure led to increased expression of ovarian BMP2 mRNA, and the effect of E2 could not be suppressed by LDN 193189 (LDN). Either BMP2 or E2 stimulated PF formation without inducing apoptosis. RNAseq analysis of ovaries exposed to exogenous BMP2 or E2 revealed differential expression of several thousand genes. Most of the differentially expressed genes (DEG), which were common between BMP2 or E2 treatment demonstrated concordant changes, reinforcing the idea of cooperativity between E2 and BMP2 during PF formation. Further, we have Identified E2, in cooperation with BMP2, could affect the expression of three major transcription factors GATA2, GATA4 and EGR2 and one serine protease, hepsin in preGC during PF formation. Taken together, results of this study suggest that E2 and BMP2 may regulate ovarian gene expression that promote somatic cells to preGC transition and PF formation in the mouse ovary.

2022-05-31 | GSE197122 | GEO

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