Gene expression in BM niche populations
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA429030 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6450350.fastq.gz | Fastqsanger.gz | |||
| SRR6450360.fastq.gz | Fastqsanger.gz | |||
| SRR6450351.fastq.gz | Fastqsanger.gz | |||
| SRR6450361.fastq.gz | Fastqsanger.gz | |||
| SRR6450352.fastq.gz | Fastqsanger.gz |
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Project description:We report transcriptome profiling of bone marrow niche subsets at the population level. Additionally, we report trascriptional changes in lymphoid -primed multipotential progenitors in the absence of vascular DLL4.
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Project description:Background. Multiple myeloma (MM) cells depend on the bone marrow (BM) niche for growth and survival. However, the tumor genes regulated by the niche are largely unknown. Design and Methods. BM aspiration samples were obtained from MM-patients with a high tumor load. Gene expression profile (GEP) was recorded immediately following aspiration and at subsequent time points. Identification of niche-regulated genes relied on spontaneous gene modulation following loss of niche regulation. Results. Compared to the reference samples fixed immediately following aspiration, the BM samples fixed after longer delay acquired numerous changes in GEP. The top modulated genes included a common subset of ~ 60 genes displaying prompt and sustained “switch” in expression consistently, among which were oncogenes (FOS, JUN) and genes regulating homing (CD69, RGS1), expansion and angiogenesis (AREG, PTGS2, RGS2, NR4A2). Interestingly, the “switch” in GEP was reversible and turned “off” and “on” in culture conditions resuming cell-cell-matrix contact versus re-spread into suspension, respectively. Moreover, the resuming of contact prolonged the survival of the tumor cells out-of-niche and the regression of the “contactless switch” was followed by induction of a new set of genes this time mostly encoding extracellular proteins, including angiogenic factors (IL8, CXCL5), extracellular-matrix proteins (SPP1, FN1), chemokines (CXCL5, CCL2, CCL20) and growth factors (CCL2, IL6). Conclusions. Our dataset, being unique in authentic expression design, uncovered contact-regulated genes capable of controlling homing, expansion and tumorigenesis. The adaptive response of the tumor cells to culture conditions deficient of integral niche components (e.g., vascular vessels) uncovered inducible niche-regulating tumor genes.
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Project description:Bone marrow (BM) mesenchymal stem and progenitor cells (MSPCs) are a critical constituent of the hematopoietic stem cell (HSC) niche. Previous studies have suggested that the zinc-finger epithelial-mesenchymal transition transcription factor Snai2 (also known as Slug) regulated HSCs autonomously. Here, we show that Snai2 expression in the BM is restricted to the BM stromal compartment where it regulates the HSC niche. Germline or MSPC-selective Snai2 deletion reduces the functional MSPC pool, their mesenchymal lineage output, and impairs HSC niche function during homeostasis and after stress. RNA-sequencing analysis revealed that Spp1 (osteopontin) expression is markedly upregulated in Snai2-deficient MSPCs. Genetic deletion of Spp1 in Snai2-deficient mice, rescues MSPCs’ functions. Thus, SNAI2 is a critical regulator of the transcriptional network maintaining MSPCs by the suppression of osteopontin expression.
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Project description:Leukemia stem cells (LSC) are not eradicated in chronic myeloid leukemia (CML) patients responding to tyrosine kinase inhibitor treatment. Bone marrow (BM) mesenchymal niches play an essential role in hematopoietic stem cell (HSC) maintenance. Here, we examined leukemia-induced alterations in mesenchymal progenitor populations using a murine CML model. 6C3+ stroma-forming progenitors were increased in CML BM, and demonstrated enhanced LSC but reduced HSC support compared to their normal counterparts. CML 6C3 cells showed enhanced TNFa-related gene signatures, and upregulated CXCL1 expression. TNFα signaling contributed to expansion and increased CXCL1 expression by 6C3 cells in CML BM. The CXCL1 receptor CXCR2 was upregulated in in LSC, and CXCR2 inhibition significantly reduced LSC growth both in vitro and in vivo. In conclusion, TNFα-induced alterations in stromal progenitors in CML BM result in enhanced CML LSC growth via CXCL1-CXCR2 signaling. Targeting this axis represents a novel therapeutic strategy to inhibit BM niche-protected LSC.
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Project description:The bone marrow (BM) niche comprised of BM endothelial cells (BMECs) and LepR+ mesenchymal stromal cells (MSCs), plays a critical role in preserving the fitness of hematopoietic stem cells (HSCs). Aging is associated with defects in the BM niche that impair their ability to support HSC activity. However, mechanisms underlying age-related defects in the BM niche remain poorly understood. In this study, we identify BM niche derived Netrin-1 (NTN1) as a critical regulator of BM niche cell fitness during aging. Conditional deletion of NTN-1 specifically within BM MSCs or BMECs of young mice resulted in premature aging phenotypes within the BM niche including increased vascular leakiness, hypoxia, DNA damage and adiposity. On the other hand, supplementation of aged mice with NTN1 resulted in restoration of these hallmark niche defects and a rejuvenation of HSC activity. Mechanistically, we identify NTN1 as a critical regulator of DNA Damage Response (DDR) within BM niche cells and HSCs. In this experiment, RNA Seq analysis was performed on BM MSCs and BMECs following conditional deletion of NTN1 within BMECs or MSCs to characterize transcriptional alterations within BM niche cells resulting from a deficiency of niche derived NTN1.
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Project description:The bone marrow (BM) niche comprised of BM endothelial cells (BMECs) and LepR+ mesenchymal stromal cells (MSCs), plays a critical role in preserving the fitness of hematopoietic stem cells (HSCs). Aging is associated with defects in the BM niche that impair their ability to support HSC activity. However, mechanisms underlying age-related defects in the BM niche remain poorly understood. In this study, we identify BM niche derived Netrin-1 (NTN1) as a critical regulator of BM niche cell fitness during aging. Conditional deletion of NTN-1 specifically within BM MSCs or BMECs of young mice resulted in premature aging phenotypes within the BM niche including increased vascular leakiness, hypoxia, DNA damage and adiposity. On the other hand, supplementation of aged mice with NTN1 resulted in restoration of these hallmark niche defects and a rejuvenation of HSC activity. Mechanistically, we identify NTN1 as a critical regulator of DNA Damage Response (DDR) within BM niche cells and HSCs. In this experiment, RNA Seq analysis was performed on BM MSCs and BMECs following conditional deletion of NTN1 within BMECs or MSCs to characterize transcriptional alterations within BM niche cells resulting from a deficiency of niche derived NTN1.
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Project description:Gene expression profiling of adult chondrocyte populations
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Project description:The bone marrow (BM) niche comprised of BM endothelial cells (BMECs) and LepR+ mesenchymal stromal cells (MSCs), plays a critical role in preserving the fitness of hematopoietic stem cells (HSCs). Aging is associated with defects in the BM niche that impair their ability to support HSC activity. However, mechanisms underlying age-related defects in the BM niche remain poorly understood. In this study, we identify BM niche derived Netrin-1 (NTN1) as a critical regulator of BM niche cell fitness during aging. Conditional deletion of NTN-1 specifically within BM MSCs or BMECs of young mice resulted in premature aging phenotypes within the BM niche including increased vascular leakiness, hypoxia, DNA damage and adiposity. On the other hand, supplementation of aged mice with NTN1 resulted in restoration of these hallmark niche defects and a rejuvenation of HSC activity. Mechanistically, we identify NTN1 as a critical regulator of DNA Damage Response (DDR) within BM niche cells and HSCs. In this experiment, RNA Seq analysis was performed on BM MSCs derived from young (3 month old) and aged (18 month old) mice to characterize transcriptional alterations within BM MSCs during aging.
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