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BioID using Rac1G15A in human podocyte

ABSTRACT: Previous studies showed that Rac1, one of the prototypical Rho GTPases, is critical for the normal development and health of podocytes. However, the upstream regulatory mechanism for Rac1 activity in podocytes is unknown. In the current study, BioID was used to identify interactors of Rac1 in human podocytes

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Jun Matsuda

LAB HEAD: Tomoko Takano

PROVIDER: PXD023718 | Pride | 2023-03-11

REPOSITORIES: Pride

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			Action	DRS
	Mirela_Takano_BirA_-T_3_09.dat	Other
	Mirela_Takano_BirA_-T_3_09.mgf	Mgf
	Mirela_Takano_BirA_-T_3_09.raw	Raw
	Mirela_Takano_BirA_-T_3_10.dat	Other
	Mirela_Takano_BirA_-T_3_10.mgf	Mgf

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1 - 5 of 12

Publications

CdGAP maintains podocyte function and modulates focal adhesions in a Src kinase-dependent manner.

Matsuda Jun J Greenberg Dina D Ibrahim Sajida S Maier Mirela M Aoudjit Lamine L Chapelle Jennifer J Baldwin Cindy C He Yi Y Lamarche-Vane Nathalie N Takano Tomoko T

Scientific reports 20221104 1

Rho GTPases are regulators of the actin cytoskeleton and their activity is modulated by GTPase-activating proteins (GAPs) and guanine nucleotide exchanging factors (GEFs). Glomerular podocytes have numerous actin-based projections called foot processes and their alteration is characteristic of proteinuric kidney diseases. We reported previously that Rac1 hyperactivation in podocytes causes proteinuria and glomerulosclerosis in mice. However, which GAP and GEF modulate Rac1 activity in podocytes ...[more]

PMID: 36333327

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Glucocorticoid therapy regulates podocyte motility by inhibition of Rac1

Project description:Nephrotic syndrome (NS) occurs when the glomerular filtration barrier becomes excessively permeable leading to massive proteinuria. In childhood NS, dysregulation of the immune system has been implicated and increasing evidence points to the central role of podocytes in the pathogenesis. Children with NS are typically treated with an empiric course of glucocorticoid (Gc) therapy; a class of steroids that are activating ligands for the glucocorticoid receptor (GR) transcription factor. Although Gc-therapy has been the cornerstone of NS management for decades, the mechanism of action, and target cell, remain poorly understood. We tested the hypothesis that Gc acts directly on the podocyte to produce clinically useful effects without involvement of the immune system. In human podocytes, we demonstrated that the basic GR-signalling mechanism is intact and that Gc induced an increase in podocyte barrier function. To gain mechanistic insight we performed RNA microarray and ChIP-sequencing and identified Gc regulation of motility genes.

2017-07-17 | E-MTAB-5235 | biostudies-arrayexpress

Role of calcium/calmodulin-dependent kinase type IV in podocyte function in lupus nephritis

Project description:Kidney podocytes and their slit diaphragms contribute to prevent urinary protein loss. T cell from patients with systemic lupus erythematosus display increased expression of calcium/calmodulin kinase IV (CaMKIV). Here we evaluated the functional role of CaMKIV in lupus nephritis (LN) using kidney biopsy specimens and human podocyte cell line (AB8/13). We found that exposure of podocytes to IgG from LN patients resulted in entry of IgG into the cytoplasm. CaMKIV expression was found to be increased in podocytes of LN kidney biopsy specimens and exposure to IgG from LN patients. IgG entered podocytes using the FcRn receptor because when podocytes where treated with FcRn siRNA less IgG was found in the cytoplasm. The DNA microarray studies of podocytes exposed to LN IgG revealed that genes that are related to the activation of immune cells or podocyte damage were upregulated. These genes included CD86, CaMKIV, PTPN22, PDE5A, CD47 and MALT1. Interestingly, CD86 expression decreased after silencing CaMKIV in podocytes. Also, in situ hybridization experiments showed that the expression of CD86 was reduced in podocytes from MRL/lpr.camkivM-bM-^HM-^R/M-bM-^HM-^R mice. IgG from LN patients may enter podocytes through the FcRn and causes the upregulation of a distinct set of genes which may alter podocyte function. Upregulation of CaMKIV appears to precede that of genes known to be linked to podocyte damage such as CD86. These findings may indicate that inhibition of CaMKIV may prove of clinical use in patients with LN. IgG Purification Kits (Dojindo Molecular Technologies, Inc.) are used for isolation and purification of immunoglobulin G of healthy and normal individual according to the manufacturerM-bM-^@M-^Ys protocol. Flow through the column was used for non IgG binding samples. Cultured human podocytes with IgG purified from sera of normal individuals and LN patient for 24 hr were collected for RNA.

2014-08-01 | E-GEOD-55768 | biostudies-arrayexpress

Mouse Podocyte Proteome - ARP3 Controls the Podocyte Architecture at the Kidney Filtration Barrier

Project description:Label-free expression proteomics analysis of FACS-sorted mouse podocytes versus non-podocytes

2018-12-14 | PXD010601 | Pride

Molecular fingerprint of the podocyte reveals novel gene regulatory networks

Project description:The thorough characterization of the transcriptome of endogenous podocytes has been hampered by low yields of cell isolation procedures. Here we introduce a double fluorescent reporter mouse model combined with an optimized bead perfusion protocol and efficient single cell dissociation yielding more than 500,000 podocytes per mouse allowing for global, unbiased downstream applications. Combining mRNA transcriptional profiling revealed programs of highly specific gene regulation tightly controlling cytoskeleton, cell differentiation, endosomal transport and peroxisome function in podocytes. Strikingly, the analyses further predict that these podocyte-specific gene regulatory networks are accompanied by alternative splicing of respective genes. In summary, the presented M-bM-^@M-^XomicsM-bM-^@M-^Y approach will facilitate the discovery and integration of novel gene, protein and organelle regulatory networks that deepen our systematic understanding of podocyte biology. To compare gene expression of glomerulus podocytes versus non-podocytes 5 replicates of 4 pooled mice were used. Data were normalized by robust multi-chip analysis. Exon expression values were summarised to the core meta probesets, as defined by Affymetrix, using the oligo library from R.

2012-11-30 | E-GEOD-39441 | biostudies-arrayexpress

ADCK4 knockout Human podocyte iTRAQ

Project description:Although identification of single gene mutations associated with SRNS have yielded insights into pathogenic mechanisms and localized its pathogenesis to glomerular podocytes, the disease mechanisms of SRNS remain obscure. ADCK4 mutations usually manifest as steroid-resistant nephrotic syndrome, and cause coenzyme Q10 (CoQ10) deficiency.The reduced form of CoQ (QH2) plays a role as a potent lipid-soluble antioxidant, scavenging free radicals and preventing lipid peroxidative damage. Although ADCK4 KO in itself did not affect the viability of cultured podocytes, we examined cell viability upon arachidonic acid (AA) treatment because CoQ-deficient yeast mutants were found to be more sensitive to polyunsaturated fatty acids such as AA, which are prone to autoxidation and breakdown into toxic products. To comprehensively understand the molecular changes induced by the KO of ADCK4, we performed proteomic analysis and quantified protein abundance changes by MS-based proteomics using isobaric tag for relative and absolute quantification (iTRAQ) in podocytes with and without AA treatment.

2021-09-09 | PXD016725 | Pride

Gene expression in a conditionally immortalized mouse podocyte cell line

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

Deep mapping of the mouse podocyte proteome

Project description:We analyzed the proteome of mouse FACS-sorted podocytes. We compared podocytes ("green cells") with non-podocyte ("red cells") cells of the glomerulus.

2018-06-21 | PXD003306 | Pride

Deep proteomic mapping of the human podocyte proteome

Project description:We subjected differentiated and undifferentiated podocytes to deep proteomics analysis by tryptic digestion and SCX fractionation.

2018-05-01 | PXD007075 | Pride

Comparison of Glomerular and Podocyte mRNA Profiles in eNOS-/- Diabetic Mice Induced by Streptozotocin

Project description:We compared mRNA profiles of isolated glomeruli versus sorted podocytes between diabetic and control mice. IRG mice crossed with eNOS-/- mice were further bred with podocin-rTTA and TetON-Cre mice to permanently label podocytes before the diabetic injury. Diabetes was induced by injection of streptozotocin. mRNA profiles of isolated glomeruli and sorted podocytes from diabetic and control mice at 10 weeks after induction of diabetes were examined. Consistent with the previous reports, expression of podocyte-specific markers in the glomeruli were down-regulated in the diabetic mice compared to controls. However, these differences disappeared when mRNA levels were corrected for podocyte number per glomerulus. Interestingly, the expression of these markers was not altered in sorted podocytes from diabetic mice, suggesting that the reduced expression of podocyte markers in isolated glomeruli is likely a secondary effect of reduced podocyte number, rather than the loss of differentiation markers. Analysis of the differentially expressed genes in diabetic mice also revealed distinct up-regulated pathways in the glomeruli (mitochondrial function and oxidative stress) and podocytes (actin organization). In conclusion, our data suggest that podocyte-specific gene expression in transcriptome obtained from the whole glomeruli may not represent those of podocytes in the diabetic kidney. We compared mRNA profiles of isolated glomeruli versus sorted podocytes between diabetic and control mice.

2016-03-16 | E-GEOD-79291 | biostudies-arrayexpress

Study of APOL1-containing complexes in podocytes

Project description:The C-terminal variants G1 and G2 of apolipoprotein L1 (APOL1) confer human resistance to the sleeping sickness parasite Trypanosoma rhodesiense, but also increase the risk of developing kidney disease. APOL1 and APOL3 are death-promoting proteins associated with endoplasmic reticulum and Golgi membranes. We report that in podocytes, either expression of APOL1 devoid of C-terminal helix (APOL1) or deletion of APOL3 (APOL3 KO) induce actomyosin reorganization linked to inhibition of phosphatidylinositol-4-phosphate (PI(4)P) synthesis by the Golgi PI(4)-kinase IIIB (PI4KB). Both APOL1 and APOL3 form K+ channels, but only APOL3 exhibited Ca2+-dependent binding to neuronal calcium sensor-1 (NCS-1), promoting NCS-1/PI4KB interaction that strongly activates PI(4)P synthesis. APOL1 C-terminal deletion or mutations increased APOL1 binding to APOL3, affecting APOL3 interaction with NCS-1. Since podocytes of G1 and G2 patients exhibited an APOL1/APOL3KO-like phenotype, APOL1 C-terminal variants may induce kidney disease by preventing APOL3 from activating PI4KB, resulting in actomyosin reorganization of podocytes.

2020-03-19 | PXD016851 | Pride

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