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Transcriptomic analysis of kidney cortex following podocyte-loss of Klf4

ABSTRACT: The goal of this study was to identify transcriptomic changes of mouse kidney cortex in mice with podocyte-specific deletion of Kruppel-like factor 4, a zinc-finger transcription factor.

ORGANISM(S): Mus musculus

PROVIDER: GSE149818 | GEO | 2021/09/22

REPOSITORIES: GEO

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Transcriptomic analysis of glomeruli following podocyte-loss of Klf4

Project description:The goal of this study was to identify transcriptomic changes of mouse glomeruli in mice with podocyte-specific deletion of Kruppel-like factor 4, a zinc-finger transcription factor.

2021-09-22 | GSE149817 | GEO

Transcriptomic analysis of kidney cortex following podocyte-loss of Klf4

Project description:Transcriptomic analysis of kidney cortex following podocyte-loss of Klf4

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Podocyte-specific induction of Krüppel-like factor 15 restores differentiation markers and attenuates kidney injury in proteinuric kidney disease

Project description:Podocyte injury is the hallmark of proteinuric kidney diseases, such as Focal Segmental Glomerulosclerosis and Minimal Change Disease. Therapeutic strategies in the management of proteinuric diseases are limited. Although agents such as glucocorticoids, cyclosporine, and rituximab have direct effects on the podocyte by stabilizing its actin cytoskeleton, these drugs are riddled with systemic toxicity and off-target effects that hinder their chronic use. We previously demonstrated that the loss of the kidney-enriched zinc finger transcription factor, Krüppel-like factor 15 (KLF15), increases susceptibility to proteinuric kidney disease as well as attenuates the salutary effects of retinoic acid and glucocorticoids in the podocyte. Here, we show that podocyte-specific induction of KLF15, using the tetracycline-inducible system, attenuated podocyte injury, glomerulosclerosis, tubulointerstitial fibrosis and inflammation, while improving renal function and overall survival in HIV-1 transgenic mice. Enrichment analysis of mRNA sequencing of isolated glomerular extracts from this model shows that podocyte-specific induction of KLF15 activates pathways involved in stabilization of actin cytoskeleton, focal adhesion, and podocyte differentiation. Transcription factor enrichment analysis, with further experimental validation, suggests that KLF15 activity is in part mediated by Wilms Tumor 1 (WT1), a transcription factor known to be critical for podocyte differentiation. Further, we confirmed the benefits of podocyte-specific induction of KLF15 in the adriamycin-induced proteinuric murine model. Collectively, these observations suggest that induction of KLF15 might be a potential therapeutic target in the treatment of proteinuric kidney disease.

2018-08-02 | GSE117987 | GEO

Transcriptomic analysis of glomeruli and kidney cortex following podocyte-loss of Klf4

Project description:Transcriptomic analysis of glomeruli and kidney cortex following podocyte-loss of Klf4

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Transcriptomic analysis of glomeruli and kidney cortex following podocyte-loss of Klf4

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-09-22 | GSE149819 | GEO

Transcriptomic analysis of glomeruli following podocyte-loss of Klf4

Project description:Transcriptomic analysis of glomeruli following podocyte-loss of Klf4

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Gene expression profile at single cell level of podocyte-specific I-PpoI expressing mice kidney cortex

Project description:To investigate the alterations in cell populations in the kidney after podocyte DNA DSBs, we performed single-cell RNA sequencing (scRNA-seq) on the renal cortex of 12-week-old podocyte-specific I-PpoI expressing mice that had not yet developed glomerulosclerosis or fibrosis.

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Transcriptional Landscape of Cells of Renin Lineage Following Podocyte Depletion

Project description:Renin producing cells of the juxtaglomerulus, herein called cells of renin lineage (CoRL), have garnered recent interest for their propensity to act as a progenitor sink for various kidney cell types including podocytes. Despite recent advances, the process of transdifferentiation of CoRL to podocytes is poorly understood. In this study, we employed a transgenic mouse line which permanently labels CoRL with ZsGreen fluorescent protein, allowing for isolation by fluorescence-activated cell sorting. At 5 days following induction of abrupt podocyte ablation via anti-podocyte sheep IgG, mice were sacrificed and CoRL were isolated by FACS. RNA was subsequently analyzed by microarray. Gene set enrichment analysis (GSEA) was performed and revealed that CoRL display a distinct phenotype following podocyte ablation, primarily consisting of downregulation of metabolic processes and upregulation of immuno-modulatory processes. Additionally, RNA-biology and cell cycle-related processes were also upregulated. Changes in gene expression or activity of a core set of transcription factors including HNF1 and E2F were identified through changes in enrichment of their respective target genes. However, integration of results from transcription factor and canonical pathway analysis indicated that ERR1 and PU-box family members may be the major contributors to the post-podocyte ablation phenotype of CoRL. Finally, top ranking genes were selected from the microarray-based analysis and confirmed by qPCR. Collectively, our results provide valuable insights into the transcriptional regulation of CoRL following abrupt podocyte ablation.

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Project description:The goal of this study was to identify genome-wide chromatin accessibility changes caused by podocyte specific overexpression of KLF6 in STZ + UNX induced diabetic mouse model.

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Role of KLF6 in shaping macrophage inflammatory response

Project description:Kruppel-like transcription factor 6 (KLF6) is a member of zinc-finger family transcription factors that regulate critical cellular processes including development, differentiation, proliferation, and programmed cell death. Alterations in KLF6 expression or function has been associated with the pathogenesis of numerous human ailments, including inflammatory bowel diseases, cancer, hepatic steatosis, and hepatic fibrosis.

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