Mouse C2C12 cells treated with/without hBMP2
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Atsushi Yamada
PROVIDER: E-GEOD-33567 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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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. We used cDNA microarrays to elucidate regulators of BMP-2-induced osteoblast differentiation.
2012-03-29 | E-GEOD-36925 | biostudies-arrayexpress
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
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, while it inhibits myogenic differentiation in C2C12 cells.
2011-11-11 | GSE33567 | GEO
Project description:Bone morphogenetic proteins (BMPs) are extracellular signaling molecules that belong to the transforming growth factor beta (TGF-β) superfamily. By regulating target gene transcription, BMPs control various cellular processes, such as proliferation, differentiation, apoptosis and migration. In addition, rBMP2 was used to observe BMP signaling in treatment of ovarian cancer cell line SK-OV-3. We attempted to address the possible roles of BMP signaling by inhibiting a wide-range of downstream pathways using a small molecule inhibitor of type I BMPRs, dorsomorphin. The potential utility of this molecule as a molecular inhibitor of BMP signaling in treatment of ovarian cancer cell line SK-OV-3 was also evaluated. SK-OV-3 cells were incubated in 12 separate culture dishes, 3 dishes with PBS, 3 dishes with recombinant BMP2 (rBMP2) (100 ng/ml), 3 dishes with DM (5 μM) and 3 dishes with recombinant BMP2 (rBMP2) (100 ng/ml) plus DM (5 μM) in the culture medium for 24 hours prior to the analysis.
2014-08-07 | E-GEOD-60135 | biostudies-arrayexpress
Project description:Both bone morphogenetic proteins (BMPs) and histone deacetylases (HDACs) have previously been established to play a role in the development of the three major cell types of the central nervous system: neurons, astrocytes, and oligodendrocytes. We have previously established a connection between these two protein families, showing that HDACs suppress BMP-promoted astrogliogenesis in the embryonic striatum. Since HDACs act in the nucleus to effect changes in transcription, an unbiased analysis of their transcriptional targets could shed light on their downstream effects on BMP-signaling. Using neurospheres from the embryonic striatum as an in vitro system to analyze this phenomenon, we have performed microarray expression profiling on BMP2- and trichostatin A (TSA)-treated cultures, followed by validation of the findings with quantitative RT-PCR and protein analysis. Neurospheres from the embryonic striatum were used to analyze cellular differentiation into neurons and astrocytes in vitro. To analyze the role of BMP2 and the HDAC-inhibitor TSA in this system, neurospheres were treated with TSA or BMP2 for 24 h, and mRNA was extracted after 6 and 24 h of the respective treatment.
2012-06-30 | E-GEOD-31792 | biostudies-arrayexpress
Project description:KSRP knock-down and BMP2 treatment produce a largely overlapping reshape of the transcriptome in C2C12 cells. microRNAs (miRNAs) are essential regulators of development, physiology, and evolution with miRNA biogenesis being strictly controlled at multiple levels. Regulatory proteins, such as KH-type splicing regulatory protein (KSRP), modulate rates and timing of the enzymatic reactions responsible for maturation of select miRNAs from their primary transcripts in response to specific stimuli. Induction of myogenic miRNAs (myomiRs) is essential for muscle differentiation with KSRP phosphorylation being required to convey myogenic signals to enhanced myomiR maturation. Here we show that either KSRP silencing or Bone Morphogenetic Protein (BMP)2-signaling activation in mesenchimal C2C12 cells prevented myogenic differentiation while induced osteoblastic differentiation as revealed by the reshaping of the whole transcriptome analyzed by RNA deep-sequencing. The most striking feature common to both BMP2 signaling activation and KSRP silencing was a blockade of myomiR maturation. Our results demonstrate that phosphorylated SMAD proteins, the transducers of BMP signaling, associate with KSRP and block its interaction with primary-myomiRs. This, in turn, abrogates KSRP-dependent myomiR maturation with the knock-down of SMAD4, 5, and 9 being able to rescue KSRP function. SMAD-induced blockade of KSRP-dependent myomiR maturation, in parallel to the well known SMAD function on gene transcription, inhibits C2C12 cell differentiation into myofibers and contributes to orient cells towards osteoblast lineage. We propose that remodeling of co-regulatory complexes affecting primary-miRNA processing is a mechanism well suited to guide cell fate determination in eukaryotes. Total RNA was prepared from 1. untreated mock-transfected C2C12 cells; 2. BMP2-treated mock-transfected C2C12 cells; 3. untreated shKSRP-transfected C2C12 cells and analyzed by RNA-seq
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Project description:Enhanced BMP or canonical Wnt (cWnt) signaling are therapeutic strategies employed to enhance bone formation and fracture repair, but the mechanisms each pathway utilizes to specify cell fate of bone-forming osteoblasts remain poorly understood. Among all BMPs expressed in bone, we find that singular deficiency of Bmp2 blocks the ability of cWnt signaling to specify osteoblasts from limb bud or bone marrow progenitors. When exposed to cWnts, Bmp2-deficient cells fail to progress through the Runx2/Osx1 checkpoint and thus do not upregulate multiple genes controlling mineral metabolism in osteoblasts. Cells lacking Bmp2 after induction of Osx1 differentiate normally in response to cWnts, supporting pre-Osx1+ osteoprogenitors as a critical source and target of BMP2. Our analysis furthermore reveals Grainyhead-like 3 (Grhl3) is to date an unidentified transcription factor in the osteoblast gene regulatory network that is induced during bone development and bone repair, and acts upstream of Osx in a BMP2-dependent manner. The Runx2/Osx1 transition therefore receives critical regulatory inputs from BMP2 that are not compensated for by cWnt signaling, and this is mediated at least in part by induction and activation of Grhl3.
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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).
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Project description:Physiological pathway of bone metabolism have been characterized well relatively. But antagonic pathway are less well studied. Here we investigated a negative regulator of osteogenesis with peroxiredoxin 5 (Prdx5) knockout mice that shows delay the bone metabolism. Prdx5-deficiency triggers a drastic decrease in both osteoblast and osteoclast number and BMP2 and RANKL level in serum.
2023-02-01 | PXD020082 | Pride
Project description:Bone Morphogenetic Protein (BMP), a bone induction factor, belongs to the TGF-β superfamily, and more than 15 types of BMP family molecules have been reported in mammals. They are known to enhance osteoblast differentiation and their osteogenic effects, and also promote differentiation into chondrocytes. While the effects of BMPs on hard tissues are varied and numerous reports have been reported, only a few have reported the effects of BMPs on salivary glands. The aim of this study was to investigate the function of BMP-2 in the formation of salivary glands.
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