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Transcriptomic profiling of the myeloma bone-lining niche identifies BMP signalling as a target for bone disease

ABSTRACT: Transcriptomic profiling of the myeloma bone-lining niche identifies BMP signalling as a target for bone disease

PROVIDER: PRJNA560055 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9947480.fastq.gz	Fastqsanger.gz
	SRR9947490.fastq.gz	Fastqsanger.gz
	SRR9947500.fastq.gz	Fastqsanger.gz
	SRR9947510.fastq.gz	Fastqsanger.gz
	SRR9947481.fastq.gz	Fastqsanger.gz

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RNASeq of bone lining niche cell components from myeloma-bearing mice treated daily with small molecule LDN193189 (LDN) or vehicle control

Project description:We compare gene expression in FACS-sorted bone lining cell components (stromal progenitors, osteoprogenitors, endothelial cells) from LDN193189 vs. vehicle-treated myeloma-bearing mice, and in myeloma cells flushed from the central marrow vs. myeloma cells digested from the bone-lining niche. The myeloma model used is the murine 5TGM1 cell line injected into immunocompetent KaLwRij mice. LDN193189 is a type 1 BMP receptor inhibitor.

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Project description:Multiple myeloma is an incurable, bone marrow-dwelling malignancy that disrupts bone homeostasis causing skeletal damage and pain. Mechanisms underlying myeloma-induced bone destruction are poorly understood and current therapies do not restore lost bone mass. Using transcriptomic profiling of isolated bone lining cell subtypes from a murine myeloma model, we find that bone morphogenetic protein (BMP) signalling is upregulated in stromal progenitor cells. BMP signalling has not previously been reported to be dysregulated in myeloma bone disease. Inhibition of BMP signalling in vivo using either a small molecule BMP receptor antagonist or a solubilized BMPR1a-FC receptor ligand trap prevents trabecular and cortical bone volume loss caused by myeloma, without increasing tumour burden. BMP inhibition directly reduces osteoclastogenesis, increases osteoblasts and bone formation, and suppresses bone marrow sclerostin levels. In summary we describe a novel role for the BMP pathway in myeloma-induced bone disease that can be therapeutically targeted.

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Transcriptomic profiling of the myeloma bone-lining niche identifies BMP signalling as a target for bone disease

Project description:This SuperSeries is composed of the SubSeries listed below.

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RNASeq of bone lining niche cell components from healthy vs. myeloma-bearing mice

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Project description:Optogenetics is a rapidly advancing technology that combines photochemical, optical and synthetic biology techniques to control cellular behaviour and physiology. Combining sensitive light responsive optogenetic intervention tools with human pluripotent stem cell differentiation models has the potential to refine differentiation and unpick the processes by which morphogenetic signals direct tissue patterning, organisation and cell specification. Here, we utilised an optogenetic bone morphogenetic protein (BMP) signalling system (optoBMP) to drive chondrogenic differentiation of human embryonic stem cells (hESCs). We initially engineered light-sensitive hESCs through CRISPR/Cas9-mediated integration of the optoBMP system into the AAVS1 locus. Activation of optoBMP with blue light in lieu of BMP family growth factors during differentiation resulted in activation of BMP signalling pathway mechanisms and upregulation of a chondrogenic phenotype, with significant transcriptional differences compared to cells left in the dark. Furthermore, cells differentiated with light were capable of forming chondrogenic pellets consisting of a hyaline-like cartilaginous matrix.

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