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Transcriptomic analysis of human podocytes [total RNA]

ABSTRACT: We analyzed the transcriptomic profiles of human podocyte-like epithelial cells (HUPEC) obtained from urine of two subjects with APOL1 low-risk (G0/G0) genotypes and two subjects with APOL1 high-risk (G1/G2) genotypes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE194330 | GEO | 2022/12/21

REPOSITORIES: GEO

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Transcriptomic analysis of human podocytes [small RNA]

Project description:We analyzed the small RNA profiles of human podocyte-like epithelial cells (HUPEC) obtained from urine of two subjects with APOL1 low-risk (G0/G0) genotypes and two subjects with APOL1 high-risk (G1/G2) genotypes.

2022-12-21 | GSE194336 | GEO

APOL1 renal-risk variants induce mitochondrial dysfunction (Illumina)

Project description:To elucidate pathways whereby apolipoprotein L1 gene (APOL1) G1 and G2 variants facilitate kidney disease in African Americans, human embryonic kidney cells (HEK293) were used to establish doxycycline-inducible (Tet-on) cell lines stably expressing reference APOL1 G0 and its G1 and G2 renal-risk variants. Illumina human HT-12-v4 arrays and Affymetrix HTA 2.0 arrays were employed to generate global gene expression data with doxycycline induction. Significantly altered pathways identified through bioinformatics involved mitochondrial function; results were validated using immunoblotting, immunofluorescence and functional assays. Global gene expression profiles were performed on HEK293 Tet-on G0, G1, G2 and empty vector cells with and without Dox induction using Illumina human HT-12 v4 arrays. Another independent gene expression array system, Affymetrix HTA 2.0, was used to verify the results of Illumina arrays. Pair-wise and pattern-based analyses were applied to detect the mostly impacted pathways due to overexpression and by APOL1 genotypes.

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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.

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Cell-specific Inducible Human APOL1 Risk Variant Expression Cause Hypertension and Renal Damage

Project description:African Americans bear a disproportionate burden of hypertension (HTN) and hypertension-attributed chronic kidney disease (H-CKD). The role of Apolipoprotein L1 (APOL1) risk variants (G1 and G2) in these conditions have been proposed, but genetic and observational studies have shown inconsistent results.Here, we investigated the causal role of APOL1 risk variants using patient samples, transgenic animal models, and in vitro cellular experiments.In the human kidney, APOL1 was highly expressed by glomerular podocytes and endothelial cells. Mice with podocyte-specific expression of the APOL1 risk variant (G2APOL1), but not those with the reference allele (G0), developed severe secondary HTN following albuminuria and kidney disease. Mice expressing endothelial-specific G2APOL1 RV developed mild hypertension with aging, which exacerbated following uninephrectomy and a high-salt diet. This condition induced slight alterations in kidney function. In vitro and in vivo experiments demonstrated that the APOL1 risk variant activates the cytosolic nucleotide sensor STING, leading to increased production of endothelin 1. Notably, mice with endothelial-specific STING knock-out or those treated with an endothelin inhibitor were protected from G2APOL1 RV-mediated hypertension. These findings indicate the role of G2APOL1 in HTN development through STING and endothelin 1 activation, offering new precision therapeutics for addressing hypertension in Black communities carrying APOL1 risk variants.

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APOL1 renal-risk variants induce mitochondrial dysfunction (Affymetrix 2)

Project description:To assess differential gene expression by APOL1 renal-risk (2 risk alleles) vs. non-risk (G0G0) genotypes in primary proximal tubule cells (PTCs), global gene expression (mRNA) levels were examined on Affymetrix HTA 2.0 arrays in primary PTCs cultured from non-diseased kidney in African Americans without CKD who underwent nephrectomy for localized renal cell carcinoma. To detect differentially expressed gene profiles attributable to APOL1 renal-risk genotypes, African American primary proximal tubule cells with two APOL1 renal-risk alleles (N=5) and lacking renal-risk alleles (N=25) were included in comparisons of global gene expression.

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