Functional change of mouse skeletal stem cells correlated with the progression of osteoporosis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA886451 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21782826_1.fastq.gz | Fastqsanger.gz | |||
| SRR21782826_2.fastq.gz | Fastqsanger.gz | |||
| SRR21782827_1.fastq.gz | Fastqsanger.gz | |||
| SRR21782827_2.fastq.gz | Fastqsanger.gz | |||
| SRR21782828_1.fastq.gz | Fastqsanger.gz |
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Project description:The precise roles of chromatin organizations at osteoporosis risk loci remains largely elusive. Here we combined chromatin interaction conformation (Hi-C) profiling and self-transcribing active regulatory region sequencing (STARR-seq) to qualify enhancer activities of prioritized osteoporosis-associated SNPs. We identified 319 SNPs with biased allelic enhancer activity effect (baaSNPs) which linked to hundreds of candidate target genes through chromatin interactions across 146 loci. Functional characterizations revealed active epigenetic enrichment for baaSNPs, and prevailing osteoporosis-relevant regulatory roles for their chromatin interacted genes. Further motif enrichment and network mapping prioritized several putative key transcription factors (TFs) controlling osteoporosis binding to baaSNPs. Specifically, we selected on top ranked TF and deciphered that an intronic baaSNP (rs11202530) could allele-preferentially bind to YY2 to augment PAPSS2 expression through chromatin interactions and promote osteoblast differentiation. Our results underlined roles of TF-mediated enhancer-promoter contacts for osteoporosis, which may help better understand the intricate molecular regulatory mechanisms underlying osteoporosis-risk loci.
2023-12-29 | GSE231932 | GEO
Project description:Recent studies have shown that microRNAs (miRNAs) are implicated in the development of postmenopausal osteoporosis, implying potential biomarkers. We performed a microarray-based expression scanning to search for potential circulating miRNA biomarkers for postmenopausal osteoporosis as whole blood obtianed from patients was used. MiRNA expression in the whole blood of 23 Chinese postmenopausal women with osteopenia and that of 25 Chinese postmenopausal women with osteoporosis. After total RNA was extracted, all of the RNA extraction samples were seperately pooled into six subgroups according to the T-score measurement.
2014-12-23 | E-GEOD-64433 | biostudies-arrayexpress
Project description:Plastin 3 (PLS3), encoded by PLS3, is a newly recognized regulator of bone metabolism and mutations in the encoding gene result in severe childhood-onset osteoporosis. Since an X chromosomal gene, PLS3 mutation-positive males are typically more severely affected while females portray normal to increased skeletal fragility. Despite the severe skeletal pathology, conventional metabolic bone markers tend to be normal and are thus insufficient in diagnosing or monitoring patients. Our study aimed to explore serum microRNA (miRNA) concentrations in subjects with defective PLS3 function to identify novel markers that could differentiate subjects according to mutation status and give insight into the molecular mechanisms by which PLS3 regulates skeletal health. We analyzed fasting serum samples for a custom-designed panel comprising 192 miRNAs in 15 mutation-positive (5 males, age range 8–76 years, median 41 years) and 14 mutation-negative (6 males, 8–69 years, 40 years) subjects from four Finnish families with different PLS3 mutations. We identified a unique miRNA expression profile in the mutation-positive subjects with seven significantly up- or downregulated miRNAs (miR-93-3p, miR-532-3p, miR-133a-3p, miR-301b-3p, miR-181c-5p, miR-203a-3p, miR-590-3p; p-values 0.004–0.044).
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Project description:In the present study we analyzed the effect of primary osteoporosis on the transcriptome of human mesenchymal stem cells (hMSC; alternatively named mesenchymal stromal cells) from human bone marrow. Human MSC of elderly patients suffering from osteoporosis were isolated from femoral heads after low-energy fracture of the femoral neck. Bone marrow of age-matched, non-osteoporotic donors was obtained of femoral heads after total hip arthroplasty. Cells were isolated from human bone marrow according to the previously described protocol (Noth et al., 2002, J Orthop Res, 20/5, 1060-1069) under agreement of the local Ethics Committee of the University of Würzburg. Human MSC of elderly patients suffering from osteoporosis were isolated from femoral heads after low-energy fracture of the femoral neck. Additional criteria for confirming primary osteoporosis in these donors were vertebrae fractures and advanced age. Bone marrow of age-matched, non-osteoporotic donors was obtained of femoral heads after total hip arthroplasty due to osteoarthritis and/or hip dysplasia. RNA samples were taken from passage 1 or passage 2.
2012-02-22 | E-GEOD-35958 | biostudies-arrayexpress
Project description:<p>Backround&Aim: Dysbiosis of gut microbiota is closely related to the pathogenesis of osteoporosis (OP). This study aimed to identify probiotic candidates and gut-derived metabolites capable of ameliorating osteoporosis via modulation of bone metabolism. </p><p>Methods: Ovariectomized (OVX) rats were used to model PMOP. Multi-omics analyses, including 16S rDNA sequencing, metagenomics, and untargeted metabolomics, were conducted to characterize gut microbiota(GM) and metabolic alterations following icariin (ICA) administration. Probiotic candidates enriched by ICA treatment were screened based on microbial and metabolic profiles. The effects of P. distasonis (LPD) were evaluated via oral gavage and fecal microbiota transplantation (FMT) in pseudo-germ-free OVX rats. Fecal samples from PMOP patients were analyzed using qPCR to assess LPD abundance. In vitro assays were performed to examine the osteogenic and anti-resorptive activities of glycerophospholipid metabolites derived from LPD.</p><p>Results: ICA administration improved bone microarchitecture and mechanical strength in OVX rats, restored intestinal barrier integrity, and altered GM composition. Multi-omics analysis identified Parabacteroides distasonis as a key bacterium enriched by ICA. Oral gavage of LPD and FMT from ICA-treated donors ameliorated bone loss in pseudo-germ-free OVX rats. Quantitative PCR of fecal samples confirmed reduced LPD abundance in PMOP patients. Metabolomic profiling revealed that ICA and LPD elevated circulating levels of phosphatidylcholine (PC), lysophosphatidylethanolamine (Lyso PE), and lysophosphatidylcholine (Lyso PC), which were positively correlated with bone formation markers. In vitro, these metabolites enhanced osteoblast differentiation and suppressed osteoclastogenesis.</p><p><strong>Conclusions: </strong>ICA exerts anti-osteoporotic effects via GM modulation, in part through enrichment of LPD and its glycerophospholipid metabolites. These findings highlight LPD as a promising probiotic candidate and support the therapeutic potential of targeting the gut-bone axis in PMOP.</p><p><br></p>
2025-08-01 | MTBLS12803 | MetaboLights
Project description:Background: Osteoporosis and diabetes represent major global public health challenges. Neutrophil extracellular traps (NETs) serve as key components of the innate immune system by capturing bacteria, fungi, and parasites, thereby trapping them in local environments with high concentrations of antimicrobial agents leading to their elimination. This study aimed to identify biomarkers associated with NETs in osteoporosis with diabetes, and to explore the underlying molecular mechanisms. Methods: A transcriptomic sequencing dataset was obtained for osteoporosis combined with diabetes. The NETs-related genes (NETs-RGs) were obtained from previous literature. Biomarkers were identified through differential analysis, machine learning, and receiver operating characteristic (ROC). The identified biomarkers were further validated by qRT-PCR and ELISA. Subsequently, molecular regulatory network construction, immune infiltration analysis, enrichment analysis, and drug prediction were conducted. Results: S100A12 and SLC25A37 were identified as biomarkers. Their significant upregulation at the protein level was further confirmed by experimental validation in an independent cohort. Enrichment analysis indicated that S100A12 was significantly enriched in 68 pathways, including \"ECM receptor interaction\", \"maturity onset diabetes of the young\", and others. SLC25A37 was significantly enriched in 54 pathways, primarily including \"ribosome\", \"leishmania infection\", and \"Toll-like receptor signaling pathway\". A total of 7 immune cell types exhibited significant differences between the two groups, including neutrophils and regulatory T cells. A total of 59 miRNAs and 43 lncRNAs were predicted. Additionally, XIST-hsa-miR-146a-5p-S100A12 and XIST-hsa-miR-7-5-SLC25A37 were suggested to have potential regulatory roles in osteoporosis with diabetes. Drugs such as rimegepant and eptinezumab were associated with biomarkers. Conclusion: S100A12 and SLC25A37 were identified as biomarkers associated with NETs in osteoporosis with diabetes, providing a theoretical foundation for developing targeted treatments for osteoporosis with diabetes.
2026-01-11 | E-MTAB-16559 | biostudies-arrayexpress