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The effect of BMP4 and BMP6 stimulation on adult muscle stem cells (MuSC)

ABSTRACT: The effect of BMP4 and BMP6 stimulation on adult muscle stem cells (MuSC)

PROVIDER: PRJNA669835 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12837025.fastq.gz	Fastqsanger.gz
	SRR12837026.fastq.gz	Fastqsanger.gz
	SRR12837027.fastq.gz	Fastqsanger.gz
	SRR12837028.fastq.gz	Fastqsanger.gz
	SRR12837029.fastq.gz	Fastqsanger.gz

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The effect of BMP4 and BMP6 stimulation on adult muscle stem cells (MuSC)

Project description:Muscle development and regeneration strongly depends on extracellular cues and growth factors, which are taken up by muscle stem cells and guide them either towards proliferation and fusion or towards quiescence. Here we investigated the effect of bone morphogenetic protein (BMP) signaling on Pax7 positive adult muscle stem cells of the mouse. We discovered a cross talk between the BMP- and NOTCH-signalling pathways, leading to high upregulation upon BMP4/BMP6-stimulation of Hes1 mRNA which is a key component of the NOTCH-siganling pathway.

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The effect of BMP4/6 stimulation on adult muscle stem cells (MuSC)

Project description:The effect of BMP4/6 stimulation on adult muscle stem cells (MuSC)

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8 hours BMP6 treated vs untreated human mesenchymal stem cells (hMSC)

Project description:We have established that BMP6 is an important endogenous regulator of human osteoblast differentiation. Our preliminary experiment showed that 8 hour BMP6 treatment induced early osteoblast markers in hMSC. In this study, we used microarrays to profile the global gene expression program in hMSC induced by BMP6 treatment and further identify the early osteogenic responses to BMP6 stimulation. Keywords: Stress response

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Apelin Stimulation of the Perivascular MuSC Niche Enhances Endogenous Repair in Muscular Dystrophy

Project description:Impaired skeletal muscle stem cell (MuSC) function has long been suspected to contribute to the pathogenesis of muscular dystrophy (MD). Here we describe that defects in the endothelial cell (EC) compartment of the perivascular stem cell niche in three different types of MD are associated with inefficient mobilization of MuSCs following tissue damage. Using chemoinformatic analysis, we identified the 13 amino acid form of the peptidic hormone apelin (AP-13) as a candidate for systemic stimulation of skeletal muscle ECs. In dystrophic mice, administration of AP-13 generates a pro-myogenic EC-rich niche that supports MuSC function and markedly improves tissue regeneration, muscle strength, and physical performance. Moreover, we demonstrate that EC specific knockout of the AP-13 receptor leads to regenerative defects that phenocopy major pathological features of MD. Altogether, we provide in vivo proof-of-concept that enhancing endogenous repair by targeting the perivascular niche is a viable therapeutic avenue for MD and characterize AP-13 as a novel drug candidate for systemic treatment of stem cell dysfunction.

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Project description:Backround: Several microRNAs have been characterized to regulate the process of angiogenesis. Previously, bone morphogenetic protein 4 (BMP4) was shown to increase the proangiogenic activity of endothelial cells. Aim: In this project we investigated how the proangiogenic BMP4 effect is mediated by microRNAs. Experimental design: To investigate changes in the microRNA transcriptome in HUVECs a time course experiment (12, 18 and 24 h) was performed. HUVECs were kept in endothelial basal medium either with BMP4 (25 ng/ml) stimulation or buffer control (4 mM HCL with 0.1% bovine serum albumin). Comparison between stimulated vs. unstimulated cells at different time points. followed by a miRNA microarray analysis was performed.

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