Single cell RNA sequencing for mesenteric CD31+ cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE133512 | GEO | 2019/08/25
REPOSITORIES: GEO
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Project description:Single cell RNA sequencing for mesenteric CD31+ cells
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Project description:Renal tumors that arise in individuals with BHD Syndrome represent a molecularly distinct form of renal cancer. In addition, BHD syndrome is due to a mutation the folliculin gene (FLCN). While the folliculin gene is an important tumor suppressor gene, the molecular function of this gene is not well defined. By analyzing tumor samples that contain FLCN mutations, we demonstrate that the FLCN gene is an important regulator of mitochondrial function. Gene expression profiling of BHDS tumors and normal kidney tissues
2010-12-21 | E-GEOD-21816 | biostudies-arrayexpress
Project description:Renal tumors that arise in individuals with BHD Syndrome represent a molecularly distinct form of renal cancer. In addition, BHD syndrome is due to a mutation the folliculin gene (FLCN). While the folliculin gene is an important tumor suppressor gene, the molecular function of this gene is not well defined. By analyzing tumor samples that contain FLCN mutations, we demonstrate that the FLCN gene is an important regulator of mitochondrial function.
2010-12-21 | GSE21816 | GEO
Project description:In Birt-Hogg-Dubé (BHD) syndrome, germline mutations in the Folliculin (FLCN) gene lead to an increased risk of renal cancer. To address if FLCN is involved regulating cellular signaling pathways via protein and receptor phosphorylation we determined comprehensive phosphoproteomic profiles of FLCN-POS and FLCN-NEG human tumor cells (UOK257). UOK257 misses the folliculin (FLCN) gene, whereas UOK 257-2 harbours a lentiviral rescue of the FLCN gene. Experiment performed in duplicate. This data set is linked to PXD021346 that describes phosphoproteomics results for human renal tubular epithelial cells (RPTEC/TERT1).
2022-07-11 | PXD030237 | Pride
Project description:A major challenge in realizing regenerative treatment using freshly isolated Adipose Derived Regenerative Cells (ADRCs) is the cellular heterogeneity and donor variability. Ex vivo expanded ADRCs (=ASCs) are available at larger quantities and represent a more homogeneous population suitable for allogenic use. Emerging pre-clinical and clinical data however suggest similar, or even superior efficacy of ADRCs as compared to ASCs for indications involving (micro)vascular deficiency. Since CD31+ ADRCs lack in cultured ASCs, we hypothesized that these cells account for improvement of vascular function in the heterogenous ADRCs. Herein, we found that in patients with erectile dysfunction (ED), the number of injected CD31+ ADRCs correlates positively with erectile function 12 months after one bolus of autologous ADRCs. Comprehensive in vitro and ex vivo analyses confirmed superior pro-angiogenic and paracrine effects of human CD31+ enriched ADRCs compared to the corresponding CD31- and parent ADRCs. CD31+, CD31- and ADRCs were co-cultured in aortic ring-, as well as in ED-relevant corpus cavernousum tube formation assays, both showing a significantly higher ability of the CD31+ ADRCs to support tube development. This effect was corroborated using conditioned medium (CM), while quantitative mass spectrometric analysis suggested that this is explained by secretory pro-angiogenic proteins such as DKK3, ANGPT2, ANAX2 and VIM, all being enriched in CD31+ADRC CM. To gain further specification of the ADRC subpopulations expressing these proteins, single-cell RNA sequencing was performed and showed that transcripts of the upregulated and secreted proteins were present in 9 endothelial ADRC subsets including endothelial progenitor cells in the heterogenous non-cultured ADRCs. Our data thus suggest that the vascular benefit of using ADRCs in regenerative medicine is dictated by CD31+ ADRCs, which likely represent an improved alternative to heterogenous ADRCs as well as ASCs when aiming for vascular repair in cell therapy.
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Project description:CD31+brain endothelial cells obtained from the brain of C57BL/6 mice 1 day after ischemia (tMCAo) or control mice
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Project description:Birt-Hogg-Dube (BHD) syndrome is an autosomal dominant disorder characterized by hamartomas of skin follicles, cystic lung disease, and renal neoplasia. Affected individuals carry heterozygous mutations in Folliculin (FLCN), a tumor suppressor gene that becomes biallelically inactivated in kidney tumors by second-hit mutations. Similar to other factors implicated in kidney malignancies, Folliculin has been shown to modulate activation of mammalian target of rapamycin (mTOR). However, its precise in vivo function is largely unknown because germline deletion of Flcn results in early embryonic lethality in animal models. We here describe mice deficient in the newly characterized Folliculin-Interacting Protein 1 (Fnip1). In contrast to Flcn, Fnip1-/- mice develop normally, are not susceptible to kidney neoplasia, but display a striking pro-B cell block that is independent of mTOR activity. We show that this developmental arrest results at least in part from impaired V(D)J recombination and caspase-induced cell death, and that pre-recombined V(D)J and Bcl2 transgenes reconstitute pre-B and mature B cell populations respectively. We also demonstrate that conditional deletion of Flcn recapitulates the pro-B cell arrest of Fnip1-/- mice. Our studies thus demonstrate that the Flcn-Fnip complex deregulated in BHD syndrome is absolutely required for B cell differentiation and that it functions both through mTOR dependent and independent pathways. RNASeq data for two pro-B cell subsets (fraction B and CC') isolated from wt and Fnip1-/- mice
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Project description:Endothelial cells of xenotransplanted gene-edited porcine kidneys are important due to the initial and prolonged exposure to host immune cells. To better study this cell population kidney endothelial cell lines (KECs) were generated by double CD31+ sorting. In order to ensure the endothelial identity of the cells RNA-seq was performed on KECs and the concomitant CD31- population from the initial sort. Analysis of gene expression in KECs showed a depletion of markers associated with tubular identity (SLC34A1, SLC2A2, SLC12A1), and enrichment for markers of endothelial (PECAM1, CDH5, VWF) and kidney endothelial (EHD3, HOX87, HOX89) identity.
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Project description:The atypical chemokine receptor 4 (ACKR4)-expressing spleen endothelial cells (ECs) form a three-dimensional sinusoidal network connected via shunts to the marginal sinus and tightly surrounds the outer perimeter of the marginal zone. To better define this new vascular compartment within the red pulp of the spleen, were sorted CD31+ACKR4+ and CD31+ACKR4- EC populations, routinely yielding 92-98% cell purity and analyzed their transcriptional profiles.
2022-03-01 | GSE171335 | GEO
Project description:Birt-Hogg-Dube (BHD) syndrome is an autosomal dominant disorder characterized by hamartomas of skin follicles, cystic lung disease, and renal neoplasia. Affected individuals carry heterozygous mutations in Folliculin (FLCN), a tumor suppressor gene that becomes biallelically inactivated in kidney tumors by second-hit mutations. Similar to other factors implicated in kidney malignancies, Folliculin has been shown to modulate activation of mammalian target of rapamycin (mTOR). However, its precise in vivo function is largely unknown because germline deletion of Flcn results in early embryonic lethality in animal models. We here describe mice deficient in the newly characterized Folliculin-Interacting Protein 1 (Fnip1). In contrast to Flcn, Fnip1-/- mice develop normally, are not susceptible to kidney neoplasia, but display a striking pro-B cell block that is independent of mTOR activity. We show that this developmental arrest results at least in part from impaired V(D)J recombination and caspase-induced cell death, and that pre-recombined V(D)J and Bcl2 transgenes reconstitute pre-B and mature B cell populations respectively. We also demonstrate that conditional deletion of Flcn recapitulates the pro-B cell arrest of Fnip1-/- mice. Our studies thus demonstrate that the Flcn-Fnip complex deregulated in BHD syndrome is absolutely required for B cell differentiation and that it functions both through mTOR dependent and independent pathways.
2012-06-16 | GSE38741 | GEO