Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1077469 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27997479_1.fastq.gz | Fastqsanger.gz | |||
| SRR27997479_2.fastq.gz | Fastqsanger.gz | |||
| SRR27997480_1.fastq.gz | Fastqsanger.gz | |||
| SRR27997480_2.fastq.gz | Fastqsanger.gz | |||
| SRR27997481_1.fastq.gz | Fastqsanger.gz |
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Project description:The pathogenic effects of type 2 diabetes on bone are gaining attention, and a basic grasp of the cellular and molecular mechanisms underlying osteoimmunology is essential for diabetes-related bone disease. However, the influence of diabetes on osteoimmunology and bone metabolism in the BM microenvironment still remains unclear. We aimed to delineate the single-cell transcriptome of bone marrow cells from WT and type 2 diabetic mice and revealed a unique bone immune microenvironment in type 2 diabetic mice.
2023-09-04 | GSE212726 | GEO
Project description:Macrophage dysfunction and polarization plays key role in chronic inflammation associated with diabetes and its complications. However, the effect of diabetes on macrophage transcriptome including long non-coding RNAs is not known. Here, we analyzed global changes in transcriptome of bone marrow macrophages isolated from type 2 diabetic db/db mice and control littermates db/+ mice using high throughput RNA-seq technique. Data analysis showed that expression of genes relevant to fibrosis, cell adhesion and inflammation were altered in diabetic db/db mice relative to control db/+ mice. Furthermore, expression of several known and novel long non coding RNAs and nearby genes was altered in db/db mice. Gene ontology and IPA showed activation of signaling netwroks relevant to fibrosis, cell adhesion and inflammatory pathways . This study for the first time demonstrated that diabetes profoundly affects macrophage transcriptome including expression of long non coding RNAs and altered the levels of genes relevant to diabetes complications. Bone marrow macrophages were isolated from 12 weeks old type 2 diabetic male db/db mice and control littermates db/+ mice. These were differentiated in culture for 7-8 days in the presence of 10 ng/ml of MCSF-1 (BMMC) or 20 ng/ml of GM-CSF (BMGM). Then RNA was extracted and used for RNA-seq.
2014-09-15 | E-GEOD-54154 | biostudies-arrayexpress
Project description:Background—Diabetes is a prevalent public health problem that affects about one third of the U.S. population and leads to serious vascular complications with increased risk for coronary artery disease. How bone marrow hematopoiesis contributes to diabetes complications is incompletely understood. We thus investigated the role of bone marrow endothelial cells in diabetic regulation of inflammatory myeloid cell production. Methods and Results—In three types of mouse diabetes, we observed enhanced proliferation of hematopoietic stem and progenitor cells (HSPC) leading to augmented circulating myeloid cell numbers. Analysis of bone marrow niche cells revealed that endothelial cells in diabetic mice expressed less Cxcl12, a retention factor promoting HSPC quiescence. Transcriptome-wide analysis of bone marrow endothelial cells demonstrated enrichment of genes involved in epithelial growth factor receptor (EGFR) signaling in mice with diet-induced diabetes. To explore whether endothelial EGFR plays a functional role in myelopoiesis, we generated mice with endothelial-specific deletion of EGFR (Cdh5Cre EGFRfl/fl). Unexpectedly, we found enhanced HSPC proliferation and increased myeloid cell production in Cdh5Cre EGFRfl/fl mice compared to wild type mice with diabetes. Disrupted EGFR signaling in endothelial cells decreased their expression of the HSPC retention factor angiopoietin-1. We tested the functional relevance of these findings for wound healing and atherosclerosis, both implicated in complications of diabetes. Inflammatory myeloid cells accumulated more in skin wounds of diabetic Cdh5Cre EGFRfl/fl mice, significantly delaying wound closure. Atherosclerosis accelerated in Cdh5Cre EGFRfl/fl mice, leading to larger and more inflamed atherosclerotic lesions in the aorta. Conclusions—In diabetes, bone marrow endothelial cells participate in the dysregulation of bone marrow hematopoiesis and promote cardiovascular complications via leukocyte overproduction. Specifically, diabetes reduces endothelial production of Cxcl12, a quiescence-promoting niche factor that reduces stem cell proliferation. We also describe a previously unknown counter-regulatory pathway, in which protective endothelial EGFR signaling curbs HSPC proliferation and myeloid cell production via angiopoietin-1.
2021-03-01 | GSE128375 | GEO
Project description:The Lin-Sca1+c-Kit+ (LSK) fraction of the bone marrow (BM) comprises multipotent hematopoietic stem cells (HSCs), which are vital to tissue homeostasis and vascular repair. While diabetes affects HSC homeostasis overall, the molecular signature of transcriptome under the conditions of long-standing type 2 diabetes (T2D;>6 months) remains unexplored. We employed the strength of Next generation sequencing to to study the differential pattern of LSK transcriptome under chronic diabetes.
2024-07-30 | GSE261502 | GEO
Project description:More and more studies pointed out that BM was the primary target of diabetes mellitus-induced damage. The aim of this study was to determine whether distinct gene expression profiles are associated with altered functions of bone marrow cells in diabetes mellitus type 2 mice. We performed global gene expression analysis in the bone marrow cells of 3 diabetic mice and 3 non-diabetic mice using Affymetrix Gene Chip Mouse Gene 1.0 ST Arrays. The gene expression patterns of diabetic mice were compared with those of nondiabetic ones using fold change. Validity of microarray results was examined by quantitative RT-PCR.
2015-05-07 | GSE68619 | GEO
Project description:The Lin-Sca1+c-Kit+ (LSK) fraction of the bone marrow (BM) comprises multipotent hematopoietic stem cells (HSCs), which are vital to tissue homeostasis and vascular repair. While diabetes affects HSC homeostasis overall, the molecular signature of transcriptome under the conditions of long-standing type 2 diabetes (T2D;>6 months) remains unexplored. We employed the strength of Next generation sequencing to to study the differential pattern of LSK transcriptome under chronic diabetes.
2024-07-30 | GSE261501 | GEO
Project description:Macrophage dysfunction and polarization plays key role in chronic inflammation associated with diabetes and its complications. However, the effect of diabetes on macrophage transcriptome including long non-coding RNAs is not known. Here, we analyzed global changes in transcriptome of bone marrow macrophages isolated from type 2 diabetic db/db mice and control littermates db/+ mice using high throughput RNA-seq technique. Data analysis showed that expression of genes relevant to fibrosis, cell adhesion and inflammation were altered in diabetic db/db mice relative to control db/+ mice. Furthermore, expression of several known and novel long non coding RNAs and nearby genes was altered in db/db mice. Gene ontology and IPA showed activation of signaling netwroks relevant to fibrosis, cell adhesion and inflammatory pathways . This study for the first time demonstrated that diabetes profoundly affects macrophage transcriptome including expression of long non coding RNAs and altered the levels of genes relevant to diabetes complications.
2014-09-15 | GSE54154 | GEO
Project description:The activity of bone marrow hematopoeitic cells is tightly controlled by neurogenic innervations. As bone marrow cells mainly receive innervation from beta-3 adrenergic receptor, here we investigated the impact of beta3-adrenergic innervation on bone marrow cell transcriptome alterations. We sorted hematopoetic stem cells (HSCs) from wild type mice (control group) or Adrb3-/- mice (devoid of beta3-adrenergic receptor). Thereafter, Nanostring assessment was performed to compare the transcriptome alterations.
2020-09-23 | GSE158332 | GEO
Project description:Type I diabetes (T1D) impairs bone accrual in patients, but the mechanism is unclear. Here in a murine monogenic model for T1D, we demonstrate that diabetes suppresses bone formation resulting in a rapid loss of both cortical and trabecular bone. Single-cell RNA sequencing uncovers metabolic dysregulation in bone marrow osteogenic cells of the diabetic mice. In vivo stable isotope tracing reveals impaired glycolysis in diabetic bone that is highly responsive to insulin stimulation. Remarkably, deletion of the insulin receptor reduces cortical but not trabecular bone. Increasing glucose uptake by overexpressing Glut1 in osteoblasts exacerbates bone defects in T1D mice. Conversely, activation of glycolysis by Pfkfb3 overexpression preserves both trabecular and cortical bone mass in the face of diabetes. The study identifies defective glucose metabolism in osteoblasts as a pathogenic mechanism for osteopenia in T1D, and furthermore implicates boosting osteoblast glycolysis as a potential anabolic therapy.
2023-06-20 | GSE232737 | GEO
Project description:Type I diabetes (T1D) impairs bone accrual in patients, but the mechanism is unclear. Here in a murine monogenic model for T1D, we demonstrate that diabetes suppresses bone formation resulting in a rapid loss of both cortical and trabecular bone. Single-cell RNA sequencing uncovers metabolic dysregulation in bone marrow osteogenic cells of the diabetic mice. In vivo stable isotope tracing reveals impaired glycolysis in diabetic bone that is highly responsive to insulin stimulation. Remarkably, deletion of the insulin receptor reduces cortical but not trabecular bone. Increasing glucose uptake by overexpressing Glut1 in osteoblasts exacerbates bone defects in T1D mice. Conversely, activation of glycolysis by Pfkfb3 overexpression preserves both trabecular and cortical bone mass in the face of diabetes. The study identifies defective glucose metabolism in osteoblasts as a pathogenic mechanism for osteopenia in T1D, and furthermore implicates boosting osteoblast glycolysis as a potential anabolic therapy.
2023-06-20 | GSE232736 | GEO