Effect of levamisole on conditionally immortalized human podocytes (cihPod)
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE229250 | GEO | 2023/12/08
REPOSITORIES: GEO
Similar Datasets
Project description:In this work, we isolated and characterized a novel cell population derived from human amniotic fluid cells (hAKPC-P), and we differentiated them into podocytes. We used microarrays to study global changes in gene expression before and after differentiation in hAKPC-P and human immortalized podocytes (hIPod, positive control) and performed a detailed comparison between the different populations hAKPC-P were isolated by FACS sorting from the total human amniotic fluid cell population and differentiated into podocytes using VRADD media. Morphological, phenotypical and functional analysis were performed to assess their differentiation. To confirm the results, cells were compared with human conditionally immortalized podocytes.
2013-12-19 | E-GEOD-49439 | biostudies-arrayexpress
Project description:In this work, we isolated and characterized a novel cell population derived from human amniotic fluid cells (hAKPC-P), and we differentiated them into podocytes. We used microarrays to study global changes in gene expression before and after differentiation in hAKPC-P and human immortalized podocytes (hIPod, positive control) and performed a detailed comparison between the different populations
2013-12-19 | GSE49439 | GEO
Project description:Glomerular podocytes are highly differentiated cells that are key components of the kidney filtration units. The podocyte cytoskeleton builds the basis for the dynamic podocyte cytoarchitecture and plays a central role for proper podocyte function. Recent studies implicate that immunosuppressive agents including the mTOR-inhibitor everolimus have a protective role directly on the stability of the podocyte cytoskeleton. To elucidate mechanisms underlying mTOR-inhibitor mediated cytoskeletal rearrangements, we carried out microarray gene expression studies to identify target genes and corresponding pathways in response to everolimus. We analyzed the effect of everolimus in a puromycin aminonucleoside experimental in vitro model of podocyte injury. Upon treatment with puromycin aminonucleoside, microarray analysis revealed gene clusters involving cytoskeletal-associated pathways, adhesion, migration and extracellular matrix composition to be affected. Everolimus is capable of protecting podocytes from injury, both on the transcriptome and protein level. Rescued genes included TUBB2B and DCDC2, both involved in microtubule structure formation in neuronal cells but not identified in podocytes so far. Confirming gene expression data, Western-blot analysis in cultured podocytes showed an increase of TUBB2B and DCDC2 protein after everolimus treatment, and immunohistochemistry in healthy control kidneys confirmed a podocyte-specific expression. Microtubule-inhibitor experiments led to a maldistribution of TUBB2B and DCDC2 as well as an aberrant reorganization of the actin cytoskeleton. Tubb2bbrdp/brdp mice showed a delay in glomerular podocyte and capillary development. Taken together, our study suggests that off-target, non-immune mediated effects of the mTOR-inhibitor everolimus on the podocyte cytoskeleton might involve regulation of microtubules, revealing a potential novel role of TUBB2B and DCDC2 in glomerular podocyte development We analyzed the effect of everolimus on gene expression in a puromycin aminonucleoside experimental in vitro model of podocyte injury using microarrays
2015-09-09 | E-GEOD-66107 | biostudies-arrayexpress
Project description:Effect of levamisole on conditionally immortalized human podocytes (cihPod)
| PRJNA953637 | ENA
Project description:We identified binding sites of the Wilms' tumor suppressor protein WT1 in the mouse podocyte genome in vivo by ChIP-seq. Furthermore, we provide a podocyte transcriptome derived from primary podocytes that were isolated by FACS on mouse glomeruli. In short, we show that WT1 activates a highly specific podocyte transcriptome by binding to putative podocyte-specific enhancers and TSS of target genes. Genes bound by WT1 in podocytes include the majority of genes mutated in hereditary podocytopathies as well as components of the slit diaphragm, actin cytoskeleton, extracellular matrix, and within endocytosis pathways. Furthermore, we infer a podocyte TF network from DNA-binding motifs enriched at WT1-bound loci that includes Tead, Lmx1b, Mafb, Tcf21, and Fox-class transcription factors. Examination of transcription factor binding sites for WT1 by ChIP-seq. Transcriptome analysis of podocytes by RNA-seq.
2014-12-11 | E-GEOD-64063 | biostudies-arrayexpress
Project description:Calcimimetics such as R568 are renoprotective and the underlying mechanism is not yet fully clarified. We consider the importance of podocytes in mediating the beneficial effect of calcimimetics on kidney. Affymetrix array type Moe430_2 was used to study the effect of R-568. Analysis of differential gene expression indicates that R-568 acts antioxidative, stabilizes cytoskeleton, enhances cell cycle control and suppresses apoptosis in podocytes. This suggests that calcimimetics limit podocyte damage by antiapoptotic and cytoskeleton stabilizing effects and may thus constitute a new pharmacological approach in the prevention and treatment of glomerular disease. Podocytes treated with and without R568 were used for RNA extraction and hybridization on Affymetrix microarrays.
2010-04-16 | E-GEOD-15761 | biostudies-arrayexpress
Project description:Glomerular podocytes are highly differentiated cells that are key components of the kidney filtration units. The podocyte cytoskeleton builds the basis for the dynamic podocyte cytoarchitecture and plays a central role for proper podocyte function. Recent studies implicate that immunosuppressive agents including the mTOR-inhibitor everolimus have a protective role directly on the stability of the podocyte cytoskeleton. To elucidate mechanisms underlying mTOR-inhibitor mediated cytoskeletal rearrangements, we carried out microarray gene expression studies to identify target genes and corresponding pathways in response to everolimus. We analyzed the effect of everolimus in a puromycin aminonucleoside experimental in vitro model of podocyte injury. Upon treatment with puromycin aminonucleoside, microarray analysis revealed gene clusters involving cytoskeletal-associated pathways, adhesion, migration and extracellular matrix composition to be affected. Everolimus is capable of protecting podocytes from injury, both on the transcriptome and protein level. Rescued genes included TUBB2B and DCDC2, both involved in microtubule structure formation in neuronal cells but not identified in podocytes so far. Confirming gene expression data, Western-blot analysis in cultured podocytes showed an increase of TUBB2B and DCDC2 protein after everolimus treatment, and immunohistochemistry in healthy control kidneys confirmed a podocyte-specific expression. Microtubule-inhibitor experiments led to a maldistribution of TUBB2B and DCDC2 as well as an aberrant reorganization of the actin cytoskeleton. Tubb2bbrdp/brdp mice showed a delay in glomerular podocyte and capillary development. Taken together, our study suggests that off-target, non-immune mediated effects of the mTOR-inhibitor everolimus on the podocyte cytoskeleton might involve regulation of microtubules, revealing a potential novel role of TUBB2B and DCDC2 in glomerular podocyte development
2015-09-09 | GSE66107 | GEO
Project description:Calcimimetics such as R568 are renoprotective and the underlying mechanism is not yet fully clarified. We consider the importance of podocytes in mediating the beneficial effect of calcimimetics on kidney. Affymetrix array type Moe430_2 was used to study the effect of R-568. Analysis of differential gene expression indicates that R-568 acts antioxidative, stabilizes cytoskeleton, enhances cell cycle control and suppresses apoptosis in podocytes. This suggests that calcimimetics limit podocyte damage by antiapoptotic and cytoskeleton stabilizing effects and may thus constitute a new pharmacological approach in the prevention and treatment of glomerular disease.
2010-04-16 | GSE15761 | GEO
Project description:We identified binding sites of the Wilms' tumor suppressor protein WT1 in the mouse podocyte genome in vivo by ChIP-seq. Furthermore, we provide a podocyte transcriptome derived from primary podocytes that were isolated by FACS on mouse glomeruli. In short, we show that WT1 activates a highly specific podocyte transcriptome by binding to putative podocyte-specific enhancers and TSS of target genes. Genes bound by WT1 in podocytes include the majority of genes mutated in hereditary podocytopathies as well as components of the slit diaphragm, actin cytoskeleton, extracellular matrix, and within endocytosis pathways. Furthermore, we infer a podocyte TF network from DNA-binding motifs enriched at WT1-bound loci that includes Tead, Lmx1b, Mafb, Tcf21, and Fox-class transcription factors.
2014-12-11 | GSE64063 | GEO
Project description:The specialized glomerular epithelial cell (podocyte) of the kidney is a complex cell that is often damaged in glomerular diseases. Study of this cell type is facilitated by an in vitro system of propagation of conditionally immortalized podocytes. Here, genes that are differentially expressed in this in vitro model of podocyte differentiation are evaluated. Conditionally immortalized undifferentiated mouse podocytes were cultured under permissive conditions at 33*C. Podocytes that were differentiated at the non-permissive conditions at 37*C were used for comparison.
2010-08-28 | E-GEOD-23856 | biostudies-arrayexpress