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Genetic activation of glycolysis in osteoblasts preserves bone mass in type I diabetes [scRNA-seq]

ABSTRACT: Genetic activation of glycolysis in osteoblasts preserves bone mass in type I diabetes [scRNA-seq]

PROVIDER: PRJNA973674 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24629764.fastq.gz	Fastqsanger.gz
	SRR24629765.fastq.gz	Fastqsanger.gz
	SRR24629766.fastq.gz	Fastqsanger.gz
	SRR24629767.fastq.gz	Fastqsanger.gz
	SRR24629768.fastq.gz	Fastqsanger.gz

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Genetic activation of glycolysis in osteoblasts preserves bone mass in type I diabetes [scRNA-seq]

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

Genetic activation of glycolysis in osteoblasts preserves bone mass in type I diabetes [bulkRNA-seq]

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Genetic activation of glycolysis in osteoblasts preserves bone mass in type I diabetes

Project description:Genetic activation of glycolysis in osteoblasts preserves bone mass in type I diabetes

| PRJNA973668 | ENA

Genetic activation of glycolysis in osteoblasts preserves bone mass in type I diabetes [bulkRNA-seq]

Project description:Genetic activation of glycolysis in osteoblasts preserves bone mass in type I diabetes [bulkRNA-seq]

| PRJNA973672 | ENA

Genetic activation of glycolysis in osteoblasts preserves bone mass in type I diabetes

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

2023-06-20 | GSE232738 | GEO

RNA-seq Analysis of Wild Type and Mark3-/- mouse primary osteoblasts

Project description:Bone mineral density (BMD) is a highly heritable predictor of osteoporotic fracture. Genome wide association studies (GWAS) have identified hundreds of loci influencing BMD, but few have been functionally analyzed. In this study, we show that SNPs within a BMD locus on Chromosome 14q32.32 alter splicing and expression of PAR-1a/MARK3, a conserved serine/threonine kinase known to regulate bioenergetics, cell division and polarity. Mice lacking Mark3 either globally or selectively in osteoblasts have increased bone mass at maturity. RNA profiling from Mark3 deficient osteoblasts suggested changes in the expression of components of the Notch signaling pathway. Mark3 deficient osteoblasts exhibited greater matrix mineralization compared with controls that was accompanied by reduced Jag1/Hes1 expression and diminished downstream JNK signaling. Overexpression of Jag1 in Mark3 deficient osteoblasts both in vitro and in vivo normalized mineralization capacity and bone mass, respectively. Together, these findings reveal a mechanism whereby genetically regulated alterations in Mark3 expression perturb cell signaling in osteoblasts to influence bone mass.

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Project description:Increased expression of SIRT1 extends the lifespan of lower organisms and delays the onset of age-related diseases in mammals. Here, we show that SRT2104, a synthetic small molecule activator of SIRT1, extends both mean and maximal lifespan of mice fed a standard diet. This is accompanied by improvements in health, including enhanced motor coordination, performance, bone mineral density and insulin sensitivity associated with higher mitochondrial content and decreased inflammation. Short-term SRT2104 treatment preserves bone and muscle mass in an experimental model of atrophy. These results demonstrate it is possible to design a small molecule that can slow aging and delay multiple age-related diseases in mammals, supporting the therapeutic potential of SIRT1 activators in humans. Key words: Sirtuins, lifespan, healthspan, osteoporosis, muscle wasting, inflammation

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Project description:Bone remodeling is a highly dynamic process dependent on the precise coordination of osteoblasts and hematopoietic-cell derived osteoclasts. Emerging evidence indicates that cellular differentiation is associated with a metabolic rewiring in conjunction with the acquisition of specific effector functions. Changes in core metabolic pathways during osteoclastogenesis, however, are largely unexplored and it is unknown whether and how these processes are involved in bone homeostasis. We show that during differentiation preosteoclasts rearrange their tricarboxylic acid (TCA) cycle, a process crucially depending on both glucose and glutamine. This rearrangement is characterized by induction of immunoresponsive gene 1 (Irg1) and production of itaconate, which accumulates intra- and extracellularly. While the IRG1-itaconate axis is dispensable for osteoclast generationin vitroandin vivo, we demonstrate that itaconate stimulates osteoblasts by accelerating osteogenic differentiation, reducing proliferation and shifting ATP production from mitochondrial respiration to glycolysis. Additionally, supplementation of itaconate increases bone formation by boosting osteoblast activity in mice. Conversely,Irg1deficient mice exhibit decreased bone mass and have reduced osteoproliferative lesions in experimental arthritis. In summary, we identify itaconate, generated as a result of the metabolic rewiring during osteoclast differentiation, as a previously unrecognized regulator of the crosstalk between osteoclasts and osteoblasts

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Secretome Comparison of Mesenchymal Stromal Cells and Immature Osteoblasts

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2021-11-15 | MSV000088384 | MassIVE

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