Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13772163_1.fastq.gz | Fastqsanger.gz | |||
| SRR13772163_2.fastq.gz | Fastqsanger.gz | |||
| SRR13772164_1.fastq.gz | Fastqsanger.gz | |||
| SRR13772164_2.fastq.gz | Fastqsanger.gz | |||
| SRR13772165_1.fastq.gz | Fastqsanger.gz |
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Project description:Recent advances have taken advantage of various animal models in HSC aging research, including certain gene mutations, chemicals, and ionizing radiation (IR). To identify the underlying mechanisms and phenotype switching in HSC aging, we employed IR-induced premature HSC aging model and performed RNA-seq of HSCs from the bone marrow (BM) of mice at three months post IR and their age-matched control mice (Ctrl).
2023-08-08 | GSE211007 | GEO
Project description:The goal of this study is to do a global transcriptiome profiling by NGS (RNA-seq) of RNA from long bone (Femur) of young (2 months) and aged (22 months) mice to understand how the bone function and their regulations are different between these two groups. Since loss of bone is prevalent with aging, we tried to find out what all genes related to bone function are affected at the expression level with aging. Using this gene expression data, we further tried to establish a relation between the pathways and regulators that contribute to this loss of function with biological replicates.
2023-12-15 | GSE220679 | GEO
Project description:Bone marrow (BM) is normally maintained in an immune-privileged and anti-inflammatory state, kept in check principally by regulatory T cells (Tregs). Thus, it is reasonable to expect that Tregs will help shield hematopoietic stem cells (HSCs) from excessive inflammation and thereby counteract HSC aging. Understanding how BM Tregs are adapted to the aged BM and whether they are endowed with unique functions to modulate HSC aging will identify targets for prevention of HSC aging. To identify the phenotype switching and function variation in BM Tregs with physiological and premature aging, we performed RNA-seq of Tregs from the bone marrow of mice at three months post irradiation (IR) and their age-matched control mice (Ctrl).
2023-08-08 | GSE211136 | GEO
Project description:Aging is associated with osteoporosis and remodeling of bone marrow microenvironment, skewing hematopoiesis. Obesity may accelerate aging process. We use bulk-RNA sequencing to measure the transcriptomic changes of bone cells caused by long-term HFD feeding in aged mice, which mainly includes osteocytes and other bone marrow stromal cells.
2023-11-15 | GSE218105 | GEO
Project description:Aging is a universal biological phenomenon linked to many diseases, such as cancer or neurodegeneration. However, the molecular mechanisms underlying aging, or how lifestyle interventions such as cognitive stimulation can ameliorate this process, are yet to be clarified. Here, we performed a multi-omic profiling, including RNA-seq, ATAC-seq, ChIP-seq, EM-seq, SWATH-MS and single cell Multiome scRNA and scATAC-seq, in the dorsal hippocampus of young and old mouse subjects which were subject to cognitive stimulation using the paradigm of environmental enrichment. In this study we were able to describe the epigenomic landscape of aging and cognitive stimulation.
2023-09-29 | PXD045567 | Pride
Project description:Using oligomycin A-treated MLO-Y4 cells and primary murine aging osteocytes as a model of cells with mitochondrial dysfunction, it is demonstrated that when mitochondria are damaged, osteocytes tend to release signaling compounds including adenosine diphosphate. We identified that the nucleotide membrane receptors P2Y2 and P2Y6 transduced the ADP signal to Mfn2, a critical regulator of osteocyte mitochondrial transfer. Whole RNA sequencing (RNA-seq) analysis of mouse cortical bone showed that mitochondrial metabolism is impaired in aged osteocytes, and there are more extracellular nucleotides released into the matrix in cortical bone in aged mice as compared to that in young mice. Aging decreases expression levels of P2Y2/P2Y6 and Mfn2.
2024-01-24 | GSE235103 | GEO
Project description:Recent studies have provided links between glutamine metabolism and bone remodeling, but little is known about its role in primary osteoporosis progression. We aimed to determine the effects of inhibiting glutaminase (GLS) on two types of primary osteoporosis and elucidate the related metabolism. To address this issue, age-related and ovariectomy (OVX)-induced bone loss mouse models were used to study the in vivo effects of CB-839, a potent and selective GLS inhibitor, on bone mass and bone turnover. We also studied the metabolic profile changes related with aging and GLS inhibition in primary bone marrow stromal cells (BMSC) and that related with OVX and GLS inhibition in primary bone marrow-derived monocytes (BMM). Besides, we studied the possible metabolic processes mediating GLS blockade effects during aging-impaired osteogenic differentiation and RANKL-induced osteoclast differentiation respectively via in vitro rescue experiments. We found that inhibiting GLS via CB-839 prevented OVX-induced bone loss while aggravated age-related bone loss. Further investigations showed that effects of CB-839 treatment on bone mass were associated with alterations of bone turnover. Moreover, CB-839 treatment altered metabolic profile in different orientations between BMSC of aged mice and BMM of ovariectomized mice. In addition, rescue experiments revealed that different metabolic processes mediated glutaminase blockade effects between aging-impaired osteogenic differentiation and RANKL-induced osteoclast differentiation. Taken together, our data demonstrated the different outcomes caused by CB-839 treatment between two types of osteoporosis in mice, which were tightly connected to the suppressive effects on both aging-impaired osteoblastogenesis and OVX-enhanced osteoclastogenesis mediated by different metabolic processes downstream of glutaminolysis.
2024-06-17 | MTBLS9415 | MetaboLights
Project description:mDia1-miR146a double knockout (DKO) mice develop aging related MDS and eventually progress to AML at moribund stage. To investigate the rescue effect from IL6 deficiency, we created mDia1-miR146a-IL6 triple knockout (TKO) mice. Singel cell RNA seq was used to investigate the bone marrow cellularity change and pathway involved during the disease progression.
2022-08-01 | GSE206600 | GEO
Project description:Asrij deletion in mice causes loss of HSC quiescence, myeloid skewing, reduced p53 and increased DNA damage, features attributed to aged hematopoietic stem cells (HSCs). To identify the pathways and processes driving the observed HSC aging-like phenotypes upon asrij depletion and to compare the asrij KO transcriptome with aged wild type HSCs, we performed RNA-seq gene expression profiling of Lin- Sca-1+ c-Kit+ CD150+ CD48- stem cells isolated from asrij KO or asrij floxed (control) mouse bone marrow. Our results identify Asrij as a potential driver of aging-like alterations in HSCs and the RNA-seq based transcriptome could help identify additional aging biomarkers and develop strategies to rejuvenate aged HSCs or prevent premature HSC aging.
2022-01-06 | GSE192948 | GEO
Project description:Distinct skeletal stem/progenitor cells (SSPCs) have been identified in the bone marrow, growth plate, and periosteum, which are indispensable for the maintenance and remodeling of the adult skeleton. However, the decline of which cell types are responsible for age-related bone loss and what characteristic changes of these cells during aging remain to be determined. Here, we constructed premature skeletal aging models by depleting metalloproteinase Zmpste24 (Z24) in mice and found that Prx1-dependent, but not Osx-dependent, Z24 deletion caused significant bone loss. Single-cell RNA sequencing (scRNA-seq) revealed that Prx1-expressing cells in the periosteum (pSSPCs) and growth plate (gpSSPCs) significantly declined in progeria mice. Consistent with aggrecan (Acan) expression in gpSSPCs but not pSSPCs, Acan-linked Z24 depletion only caused trabecular bone loss. Chromatin and transcriptional profiling demonstrate that premature aged SSPCs gain apoptotic signaling pathway and mechanosensation decline. Moreover, SSPCs increased after physical exersice and Z24 depletion’s effects on cellular apoptosis and extracellular matrix expression were reverted by mechanical stimuli. Overall, this study identifies that Z24 deficiency-induced impairment of mechanosensation in SSPCs causes bone loss, shedding new insight on how physical exercise can be used to improve bone quality and prevent bone aging.
2023-08-01 | GSE207240 | GEO