Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR30129002_1.fastq.gz | Fastqsanger.gz | |||
| SRR30129002_2.fastq.gz | Fastqsanger.gz | |||
| SRR30129004_1.fastq.gz | Fastqsanger.gz | |||
| SRR30129004_2.fastq.gz | Fastqsanger.gz |
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Project description:Background: Adipose-derived stem cells (ADSCs) can differentiate into Schwann cells (SCs) at the site of nerve injury, where Schwann cell-derived exosomes (SC-Exos) are suspected to exert an induction effect. Our study aimed to induce the differentiation of ADSCs in vitro using SC-Exos and to investigate the mechanisms involved through miRNA sequencing. Methods: Subcutaneous fat was used to extract ADSCs. Exosomes were extracted from Schwann cell lines (RSC96) using ultracentrifugation. After 8 days of induction of ADSCs by SC-Exos, phenotypic characteristics were observed by examining the expression of SC markers (S100, NGFR, MPZ, GFAP) through RT-qPCR, Western blot and immunofluorescence. Additionally, miRNA sequencing was performed on induced ADSCs, followed by bioinformatic analysis and validation of the results. Results: SC-Exos were taken up by human ADSCs. The RNA and protein expression levels of S100, NGFR, MPZ and GFAP were found to be significantly higher in the SC-Exo induction group than in the uninduced group, despite no significant difference to the Dezawa’s method group, which was also consistent with the immunofluorescence results. According to the sequencing results, there were a total of 72 differentially expressed miRNAs. Bioinformatics analysis indicated that 3506 Gene Ontology terms and 98 Kyoto Encyclopedia of Genes and Genomes pathways were significantly enriched. Ten miRNAs, 6 target mRNAs and elevated expression of the PIK3CD/Akt pathway were validated by RT-qPCR or Western blot, which is consistent with the sequencing results. Conclusions: Our data suggest that SC-Exos are able to induce the differentiation of ADSCs into SCs in vitro. It is speculated that the differentially expressed miRNAs play a significant role in the differentiation process.
2022-02-13 | GSE183623 | GEO
Project description:Endothelial cells (ECs) have been reported to be a source of adipose tissue-derived stromal cells (ADSCs), and ADSCs expressing endothelial markers have been suggested to originate from ECs. To further investigate the lineage relationship between ECs and ADSCs in postnatal mice, we performed single-cell RNA sequencing (scRNA-seq) on ECs and ADSCs isolated from inguinal and gonadal white adipose tissues (IWATs and GWATs) of 12-week-old wild-type C57BL/6J mice, and analyzed the expression of endothelial markers in ADSCs.
2025-03-05 | GSE168334 | GEO
Project description:[1] Microarray analysis in the rat myocardial tissue: 124I-HIB transplanted MI model Vs. phosphate buffered saline (PBS) injected myocardial infarction (MI) model Vs. Sham operated model [2] Microarray analysis in the rat adipose derived stem cells: 124I-HIB-labeled ADSCs Vs. Unlabeled ADSCs [1] We investigated the change of gene expression profile in sham operated-, PBS injected- and 124I-HIB-labeled ADSCs transplanted myocardium in rat myocaridial infarction (MI) model. [2] We compared gene expression profile with 124I-HIB labeled ADSCs and unlabeled ADSCs in vitro.
2015-01-06 | E-GEOD-64692 | biostudies-arrayexpress
Project description:In the current investigation, a comprehensive analysis using high-throughput RNA sequencing (RNA-seq) was carried out on ADSCs obtained from donors of varying ages. 678 genes showed differential expression between ADSCs obtained from young and old donors (Y-ADSCs and O-ADSCs), with 47 of these genes being TFs. The findings indicated that 316 genes exhibited decreased expression levels, while 362 genes displayed increased expression levels in O-ADSCs in comparison to Y-ADSCs. Subsequent analyses using GO and KEGG were performed to further elucidate the roles of the identified differentially expressed genes. The GO analysis revealed that these genes are predominantly localized in the plasma membrane and extracellular region, serving as constituents of the extracellular matrix and participating in protein binding. Additionally, they are implicated in processes related to cell adhesion and signal transduction pathways. KEGG analysis indicated enrichment in pathways such as neuroactive ligand-receptor interaction, calcium signaling, pathways in cancer, ErbB signaling, and cell adhesion molecules.
2024-11-13 | GSE269853 | GEO
Project description:Mesenchymal stem cells (MSCs) therapy for sepsis has been extensively studied in the past decade, however, the treatment regimen and mechanism of action of MSCs remain elusive. Here, we attempted to understand the efficacy and mechanism of action of MSCs on rescuing mice with sepsis. A mouse model of sepsis was produced by cecal ligation and puncture (CLP). Allogeneic adipose-derived MSCs (ADSCs) were administered by intravenous infusion at 6 h after CLP, and dose-related effects of ADSCs on these mice were determined by survival rate, histopathological changes, biochemical and coagulation parameters, bacterial load, and plasma levels of endotoxin and inflammatory cytokines. The tissue distribution of intravenously infused ADSCs in septic mice was investigated by pre-labeling ADSCs with the lipophilic membrane dye PKH26. RNA sequencing analysis was performed to assess the transcriptional changes in peripheral blood mononuclear cells (PBMCs) and the liver. A significant therapeutic effect of ADSCs at a dose of 2×107 cells/kg in septic mice was evidenced by a remarkable reduction in mortality (36% vs 9% survival rate), blood bacterial burden, systemic inflammation, and multiple organ damage. In contrast, ADSCs at a lower dose (1×107 cells/kg) failed to achieve any beneficial outcomes, while ADSCs at a higher dose (4×107 cells/kg) caused more early death within 24 hours after CLP, retaining a steady survival rate of 21% thereafter. PKH26-labeled ADSCs were predominantly localized in the lungs of septic mice after intravenous infusion, with only a smaller proportion of PKH26-positive signals appearing in the liver and spleen. RNA-sequencing analysis identified that insufficient phagocytic activity of PBMCs in addition to a hyperactivation of the hepatic immune response was responsible for the ineffectiveness of low-dose ADSCs therapy, and acute death caused by high-dose ADSCs infusion was associated with impaired coagulation signaling in PBMCs and exacerbated hepatic hypoxic injury. Our findings demonstrate a dose-specific effect of ADSCs on the treatment of sepsis due to dose-related interactions between exogenous stem cells and the host’s microenvironment. Therefore, a precise dosing regimen is a prerequisite for ADSCs therapy for sepsis.
2022-10-05 | GSE214746 | GEO
Project description:Adipose-derived stromal cells (ADSCs) represent a promising stem cell source for tissue engineering and cell based therapy. However, long-term in vitro expansion of ADSCs impede stemness maintaining, partly attributed to deprivation of their original microenvironment. Incompetent cells largely limit the therapeutic effects in ADSCs based clinical use. Therefore, reconstructing a more physiologically and physically relevant niche is an ideal strategy to settle this issue and therefore facilitates their extensive applications in clinical. Here, we transplanted separated ADSCs to local subcutaneous adipose tissues of nude mice as an in vivo cell culture model. We found transplanted ADSCs maintained the primitive morphologies, showed improved proliferation and delayed senescence when compared to cells in conventional incubator. Significantly increased expression of stemness-related markers and multi-lineage differentiation abilities were further observed in in vivo cultured ADSCs. At last, sequencing results revealed different expression genes between ADSCs obtained from in vivo and in vitro conditions mainly located in extracellular matrix and extracellular space, which participated in regulating transcription and protein synthesis. Moreover, we found an Egr1 involved signaling pathway might exert a crucial impact on controlling stemness properties. Our findings might collectively pave the way between the bench and beside in regard of ADSCs based application.
2024-03-20 | GSE261680 | GEO
Project description:Recent researches identified the existence of adipose derived stem cells (ADSCs) in adipose tissue. Perivascular ADSCs (PV-ADSCs) locate around vasculatures and can differentiate into vascular lineages. However, the detailed cellular heterogeneity within PV-ADSCs has not been investigated. Therefore, we performed single-cell profiling of subcutaneous (S-) and perivascular (PV-) ADSCs from wild-type and obese mice. After referring to the clustering strategies from other ADSCs’ single-cell data, we provided a more comprehensive picture and trajectory, especially for PV-ADSCs. Both single-cell analysis and in vitro experiments revealed that S-ADSCs from obese mice had impaired abilities of cell migration and proliferation compared to wild-type S-ADSCs. PV-ADSCs have distinctively intrinsic properties. We uncovered 4 subpopulations of PV-ADSCs including Dpp4+, Col4a2+, Clec11a+ and Sult1e1+ cells. Notably, the differentiative function of PV-ADSCs towards vascular lineages was mainly attributed to the existence of Clec11a+ subpopulation, which highly expressed Mgp. The present study provided an integrative view of the ADSCs’ variance from the perspective of origins and obesity.
2022-02-23 | GSE172336 | GEO
Project description:Adipogenesis occurs through a specific gene program in undifferentiated fat progenitors. We hypothesized that the properties of the fat progenitors are regulated by hox genes, the developmental genes essential in different tissue stem cells. Their biased expression in white and brown fat implies roles in distinguishing the two fat types. Among 39 Hox genes, Hoxc8 is highly enriched in undifferentiated adipose tissue stem cells (ADSCs) and down-regulated in differentiated adipocytes. Forced expression of Hoxc8 suppressed adipocyte differentiation of ADSCs. Using microarrays, we investigated the effect of Hoxc8 overexpression on global transcripts in ADSCs. We compared among four groups: untreated ADSCs, adipogenic induction media (MDI)-treated ADSCs, MDI-treated ADSC-vector and MDI-treated ADSC-Hoxc8. A number of, but not all, adipogenesis-related genes are suppressed by Hoxc8. This dataset illustrates the global effect of Hoxc8, a developmental transcription factor, on the expression of adipogenesis-related genes. Gene expression was compared among untreated ADSCs (control), adipogenic induction media-treated ADSCs, adipogenic induction media-treated ADSC-vector (ADSCs transduced with control vector), and adipogenic induction media-treated ADSC-Hoxc8 (ADSCs transduced with human Hoxc8). Total RNA was isolated from ADSCs using the Qiagen RNeasy kit (Qiagen). At NimbleGen, quality and yield were verified before cDNA synthesis and Cy3-end labeling. The labeled cDNA samples were hybridized to Homo sapiens 4-Plex arrays (Roche NimbleGen, A4487001-00-01) that represent 24,000 human genes. Raw data files for each sample were normalized and background-corrected using a Robust Multi-Array Analysis as implemented by NimbleScan software. Students’ two-tail t-tests were conducted among the samples for each transcript and fold-change was determined. Transcripts whose abundance was significantly altered (P < 0.05) and an absolute fold change greater than 2 were defined as differentially regulated.
2010-06-18 | E-GEOD-22429 | biostudies-arrayexpress
Project description:The role of adipose-derived stromal stem cells (ADSCs) in BLCA progression is unclear. We investigated the effects of invasion, stemness, Epithelial-mesenchymal transition (EMT), and drug resistance of BLCA cells co-cultured with ADSCs for a long period of time. Cells were divided into six groups: ADSCs group, ADSCs:T24 group (10:1, 3:1 and 1:1 groups), ADSCs-derived conditioned medium group (CM) and T24 cell group (T24), and cells in each group were cultured to 14 days, and puromycin (puro) was added to the co-cultured cell to remove ADSCs cells without puro resistance , and then the function of T24 cells (10:1-COC, 3:1-COC and 1:1-COC) after co-culture was studied; CCK-8 assay, Transwell, Wound healing, Flow cytometry, RNA-sequencing, qRT-PCR and Western Bloting assay were used to detect cell proliferation, invasion, migration, apoptosis and cellular mRNA and protein expression levels, respectively. We unexpectedly found enhanced stemness and drug resistance of BLCA cells after prolonged contact culture with ADSCs. T24 cells after co-culture mediated cell proliferation, invasion, EMT, stemness, drug resistance and immune escape by up-regulating MDM2, mt-P53 and PD-L1, compared to CM and T24 groups. The inhibitor Atezo and CP-31398 eliminated mt-P53 and PD-L1-mediated T24 cell drug resistance and stemness, respectively. This study demonstrated that after prolonged co-culture of BLCA cells with ADSCs, the stemness, drug resistance, and immune evasion of T24 cells were dramatically enhanced.
2025-07-09 | GSE290399 | GEO
Project description:Facial infiltrating lipomatosis (FIL) is a congenital disorder characterized by unilateral facial enlargement. Although next-generation sequencing has revealed that the pathogenesis of FIL is associated with phosphatidylinositol 3-kinase catalytic subunit alpha (PIK3CA) mutations, the underlying molecular mechanisms remain undetermined. We found that the adipose tissue in FIL patients demonstrated tissue infiltration accompanied by adipocytes hypertrophy and increased lipid accumulation. All FIL-ADSCs harboured PIK3CA mutations. Compared to ADSCs obtained from normal subcutaneous adipose tissue, FIL-ADSCs exhibited a greater capacity for adipogenesis. Suppression of PIK3CA resulted in a reduction in the adipogenic potential of FIL-ADSCs. Furthermore, WX390, a novel dual-target PI3K/mTOR inhibitor, was found to impede PIK3CA-mediated adipogenesis both in vivo and in vitro. RNA-seq revealed that the expression of transient receptor potential vanilloid subtype 1 (TRPV1) was upregulated after PI3K pathway inhibition, and overexpression and activation of TRPV1 both inhibited adipogenesis of FIL-ADSCs. Our study showed that PIK3CA mutations promoted adipogenesis in FIL-ADSCs and that this effect was achieved by suppressing the expression of TPRV1. Pathogenesis experiments suggested that WX390 may serve as an agent for the treatment of FIL.
2024-06-28 | GSE253170 | GEO