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Constitutive bone marrow adipocytes suppress local bone formation and support hematopoietic stem and progenitor cells

ABSTRACT: Constitutive bone marrow adipocytes suppress local bone formation and support hematopoietic stem and progenitor cells

PROVIDER: PRJNA822382 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18568443_1.fastq.gz	Fastqsanger.gz
	SRR18568443_2.fastq.gz	Fastqsanger.gz
	SRR18568444_1.fastq.gz	Fastqsanger.gz
	SRR18568444_2.fastq.gz	Fastqsanger.gz
	SRR18568445_1.fastq.gz	Fastqsanger.gz

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Constitutive bone marrow adipocytes suppress local bone formation and support hematopoietic stem and progenitor cells

Project description:Methods: Whole distal tibial bones were collected from male control or BMAd-DTA mice at 24 weeks of age. Results: Using an optimized data analysis workflow, we mapped over 20 million sequence reads per sample to the mouse genome (UCSC mm10) and identified 22,600 transcripts in the whole distal tibial bones of control or BMAd-DTA mice using STAR with default parameters. We identified 841 genes that were significantly changed in BMAd-DTA mice; of these, 432 genes were up-regulated. Pathway analysis revealed that this gene set is enriched in ossification, extracellular matrix organization, and osteoblast differentiation pathways. Conclusion: The increased bone mass in BMAd-DTA mice appears to be secondary to enhanced bone formation, suggesting a local effect caused by depletion of BMAd.

2022-09-01 | GSE199973 | GEO

Constitutive bone marrow adipocytes suppress local bone formation.

Project description:BM adipocytes (BMAd) are a unique cell population derived from BM mesenchymal progenitors and marrow adipogenic lineage precursors. Although they have long been considered to be a space filler within bone cavities, recent studies have revealed important physiological roles in hematopoiesis and bone metabolism. To date, the approaches used to study BMAd function have been confounded by contributions by nonmarrow adipocytes or by BM stromal cells. To address this gap in the field, we have developed a BMAd-specific Cre mouse model to deplete BMAds by expression of diphtheria toxin A (DTA) or by deletion of peroxisome proliferator-activated receptor gamma (Pparg). We found that DTA-induced loss of BMAds results in decreased hematopoietic stem and progenitor cell numbers and increased bone mass in BMAd-enriched locations, including the distal tibiae and caudal vertebrae. Elevated bone mass appears to be secondary to enhanced endosteal bone formation, suggesting a local effect caused by depletion of BMAd. Augmented bone formation with BMAd depletion protects mice from bone loss induced by caloric restriction or ovariectomy, and it facilitates the bone-healing process after fracture. Finally, ablation of Pparg also reduces BMAd numbers and largely recapitulates high-bone mass phenotypes observed with DTA-induced BMAd depletion.

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MHOR002 expression: Forkhead box O transcription factors both suppress and support breast cancer progression.

Project description:MHOR002 expression: Forkhead box O transcription factors both suppress and support breast cancer progression.

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Severe infection constitutively upregulates TIMP1 in the bone marrow hematopoietic niche to support long-term enhanced myelopoiesis

Project description:Infection is able to elicit innate immunological memory by enhancing a long-term myeloid output even after the inciting infectious agent has been cleared. However, mechanisms underlying such a regulation are not fully understood. Using a mouse polymicrobial peritonitis (sepsis) model, we show that severe infection leads to increased, sustained myelopoiesis after the infection is resolved. The infection experience is imprinted in the bone marrow (BM) stromal cells, in the form of a constitutive upregulation of the tissue inhibitor of metalloproteinases 1 (TIMP1). TIMP1 antagonizes the function of ADAM10, an essential cleavage enzyme for the activation of Notch which in turn suppresses myelopoiesis. While TIMP1 is dispensable for myelopoiesis under the steady state, increased TIMP1 enhances myelopoiesis post infection. Thus, our data reveal that infection could establish an inflammatory memory in the BM niche to support a long-term enhanced output of innate immune cells.

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Reprogrammed marrow adipocytes: an unexpected role in the genesis of myeloma-induced bone disease

Project description:Multiple myeloma is characterized by osteolytic lesions caused by osteoclast-mediated bone resorption and reduced bone formation. A unique feature of myeloma is a failure of bone healing following successful treatment. Identification of increased adipocyte numbers in marrow of successfully treated patients led us to demonstrate that normal marrow adipocytes, when co-cultured with myeloma cells, are reprogrammed and produce adipokines that activate osteoclastogenesis and suppress osteoblastogenesis. These adipocytes have reduced expression of peroxisome proliferator-activated receptor γ (PPARγ) mediated by recruitment of polycomb-repressive complex 2 (PRC2) via specificity protein 1, which modifies PPARγ promoter methylation at trimethyl lysine-27 histone H3. We confirmed the importance of PPARγ methylation by demonstrating that adipocyte-specific knockout of EZH2, a member of the PRC2, prevents adipocyte reprogramming and reverses bone changes in vivo. These results define a heretofore unrecognized role for adipocytes in genesis of myeloma-associated bone disease and that reversal of adipocyte reprogramming has therapeutic implications.

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Project description:We have identified a population of adipocytes in fat tissue that arise from bone marrow-derived progenitor cells. We used microarrays to compare the global gene expression patterns of the bone marrow progenitor-derived adipocytes as well as conventional white and brown adipocytes to evaluate the relationship between these adipocyte subpopulations. Gonadal fat tissue (for white adipocytes) and intrascapular fat tissue (for brown adipocytes) was digested with collagenase and adipocytes were recovered by centrifugation/flotation. Bone marrow derived adipocytes were isolated from the adipocyte fraction of gonadal fat tissue from mice receiving bone marrow tranplants from donors expressing either green fluorescent protein (GFP) or beta-galactosidase (LacZ) by flow cytometry.

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Expression Data from Bone Marrow Progenitor-Derived Adipocytes, White Adipocytes and Brown Adipocytes.

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Reprogrammed marrow adipocytes: an unexpected role in the genesis of myeloma-induced bone disease (ChIP-Seq)

Project description:Multiple myeloma is characterized by osteolytic lesions caused by osteoclast-mediated bone resorption and reduced bone formation. A unique feature of myeloma is a failure of bone healing following successful treatment. Identification of increased adipocyte numbers in marrow of successfully treated patients led us to demonstrate that normal marrow adipocytes, when co-cultured with myeloma cells, are reprogrammed and produce adipokines that activate osteoclastogenesis and suppress osteoblastogenesis. These adipocytes have reduced expression of peroxisome proliferator-activated receptor  (PPAR) mediated by recruitment of polycomb-repressive complex 2 (PRC2) via specificity protein 1, which modifies PPAR promoter methylation at trimethyl lysine-27 histone H3. We confirmed the importance of PPAR methylation by demonstrating that adipocyte-specific knockout of EZH2, a member of the PRC2, prevents adipocyte reprogramming and reverses bone changes in vivo. These results define a heretofore unrecognized role for adipocytes in genesis of myeloma-associated bone disease and that reversal of adipocyte reprogramming has therapeutic implications.

2018-04-26 | GSE113642 | GEO

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Project description:Hematopoiesis advances cardiovascular disease by generating inflammatory leukocytes that attack the arteries, heart and brain. While it is well documented that the bone marrow niche regulates hematopoietic stem cell proliferation and hence the systemic leukocyte pool, it is less clear how cardiovascular disease affects the vasculature forming this niche. Here we show that arterial hypertension, atherosclerosis and myocardial infarction alter the anatomy and function of bone marrow vasculature. Hypertension and atherosclerosis instigated vascular fibrosis, leakage and endothelial dysfunction in the bone marrow. Myocardial infarction induced vascular leakage and bone marrow angiogenesis via Vegf signaling. Endothelial cell-specific deletion of the Vegf receptor 2 limited emergency hematopoiesis after myocardial infarction, indicating that new vasculature supports higher blood cell production. RNA-sequencing of bone marrow endothelial cells revealed inflammatory gene expression in mice with cardiovascular disease. Endothelial cell-specific deletion of interleukin 6 or versican, which were highly expressed in mice with atherosclerosis or myocardial infarction, respectively, reduced hematopoiesis and systemic myeloid cells. Taken together, cardiovascular disease affects the vascular bone marrow niche, thus influencing hematopoietic stem cell behavior and expanding innate immune cell supply to atherosclerotic plaque and ischemic myocardium. Interrupting this feed back loop may constrain cardiovascular inflammation.

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Bone marrow adipocytes fuel emergency hematopoiesis

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