ScRNAseq analysis of kidney treated with GLS1 inhibitor [scRNA-seq Kid_BPTES]
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ABSTRACT:
PROVIDER: PRJNA1284762 | ENA |
REPOSITORIES: ENA
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Project description:We employed the Chromium GEM-X single-cell RNA sequencing platform by 10x Genomics to investigate the effects of the GLS1 inhibitor, BPTES, on the kidney single-cell transcriptome of 19- to 20-month-old wild-type male mice. Previous studies have identified GLS1 as a potential senolytic reagent capable of eliminating senescent cells. Our aim was to determine which cell populations are selectively removed by GLS1 inhibition in aged mice and to assess how this intervention alters intercellular interactions across different cell types.
2025-07-02 | GSE301292 | GEO
Project description:scRNAseq analysis of lung treated with GLS1 inhibitor [scRNA-seq Lung_BPTES]
| PRJNA1281109 | ENA
Project description:We employed the Chromium GEM-X single-cell RNA sequencing platform by 10x Genomics to investigate the effects of the GLS1 inhibitor, BPTES, on the lung single-cell transcriptome of 19- to 20-month-old wild-type male mice. Previous studies have identified GLS1 as a potential senolytic reagent capable of eliminating senescent cells. Our aim was to determine which cell populations are selectively removed by GLS1 inhibition in aged mice and to assess how this intervention alters intercellular interactions across different cell types.
2025-07-02 | GSE300532 | GEO
Project description:To evaluate the roles of glutaminase 1 (GLS1) in vascular smooth muscle cells (VSMCs) phenotypic switching and aortic dissection (AD). Integrative transcriptomic analyses were performed to identify the candidate genes involved in VSMC phenotypic switching in AD. The expression of GLS1 in VSMCs was assessed by qRT-PCR, Western blot and immunofluorescence. RNA-sequencing analysis was performed to recapitulate possible changes in the transcriptome profile of GLS1 in VSMCs. We identified GLS1 as a potential regulator in AD. GLS1 expression was significantly downregulated in VSMCs from both human AD aortic tissues and mouse models. Mechanistically, down-regulation of GLS1 impaired glutamate metabolism, leading to reduced levels of glutathione and α-ketoglutarate, thereby promoting mitochondrial dysfunction and accumulation of reactive oxygen species, which activated the PI3K/AKT pathway and ultimately triggered VSMC phenotypic switching. These findings revealed a critical role of GLS1-mediated glutamate metabolism in VSMC phenotypic switching and suggest a promising therapeutic target for AD.
2026-03-20 | GSE324926 | GEO
Project description:Here, we performed single cell RNA sequencing (scRNA-seq) of human fetal kidney tissue samples from 2 individual biological specimens (13.7 and 15.4 weeks gestation). The data set is composed of approximately 10,000 cells from diverse renal lineages. Lineages captured include nephron progenitors, epithelium, stroma, immune, and endothelium.
2020-12-20 | E-MTAB-9083 | biostudies-arrayexpress
Project description:Glutaminase (GLS1) is involved in the development of Alcoholic liver disease (ALD). Protein-protein interactions underlie the biological processes impacted by GLS1. we used immunoprecipitation-mass spectrometry (IP-MS) technology and found the proteins interacted with GLS1.
2025-12-08 | PXD050603 | Pride
Project description:Human induced pluripotent stem cell-derived kidney organoids have potential for disease modelling and regenerative medicine purposes. However, they lack a functional vasculature and remain immature in in vitro culture. Here, we transplanted kidney organoids at day 7+12 of differentiation in the coelomic cavity of chicken embryos and then compared them to their respective untransplanted controls at d7+13 and d7+20 using scRNAseq and imaging modalities. We demonstrate vascularization and enhanced maturation of transplanted kidney organoids.
2022-08-05 | E-MTAB-11429 | biostudies-arrayexpress
Project description:scRNA-seq of human fetal kidney tissue
| PRJEB38382 | ENA
Project description:Human embryonic stem cell (hESC) line Man-13 was edited by CRISPR resulting in a hESC line carrying a heterozygous frameshift mutation with a premature stop codon in exon-1 of the HNF1B gene ([p.Val61Argfs*18]), functionally equivalent to a heterozygous whole-gene deletion. Kidney organoids were then created by differentiation (as per Takasato et al, 2015; Bantounas et al, 2018; Bantounas et al 2021) of this line and an isogenic non-mutant control line. Single-cell RNAseq (scRNAseq) was then performed on day-25 of differentiation to identify transcriptomic differences, as well as differences in identity and numbers of the cell populations comprising the organoids, with the aim of mechanistically explaining developmental aberrations observed in patients with mutations in this gene.
2024-04-30 | E-MTAB-13500 | biostudies-arrayexpress
Project description:Objective: Upregulation of glycolysis and glutaminolysis in the rheumatoid arthritis fibroblast-like synoviocytes (RAFLS) has already been established by existing literature . Henceforth, this study was undertaken to determine if dual inhibition of these processes by novel phytobiologic c28MS have the potential of promising synergistic therapy for rheumatoid arthritis by targeting the underlying metabolic reprogramming as existing treatment strategies for RA do not target dual inhibition. Methods: Gene associations with HK2 and GLS expression were identified by examining murine and human available scRNA-seq. The metabolic profile of FLS cells was determined by 1H magnetic resonance spectroscopy under conditions of glycolytic and glutaminolysis inhibition and HK2 and GLS1 expression was evaluated by western blot. FLS functional analysis was conducted under similar inhibitory conditions. ELISA was employed for the quantification of pivotal markers namely IL6, CCL2 and MMP3. For arthritis experiments, mice were injected with K/BxN sera on Day 0 and treated for 10 days. Results: scRNAseq data identified... Metabolomic and functional analysis revealed that c28MS had the potential of checking the aggressive behavior of RAFLS by targeting upregulated glycolysis and glutaminolysis thereby inhibiting them. Target expression remained unaffected by the action of the dual inhibitor suggesting only potential blockage. Furthermore, the compound was able to inhibit inflammatory arthritis by decreasing the clinical score and paw inflammation in the K/BxN model. Conclusion: Our findings imply that dual inhibition of glycolysis and glutaminolysis could be an effective strategy in the treatment of RA with chances of greater remission. It also suggests that targeting more than one pathway in the metabolome can be a novel treatment approach in non-cancer scenarios.
2023-04-20 | GSE230145 | GEO