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Deletion of Klotho enhancer deepens sexual dimorphism of gene expression without impacting female resistance to kidney injury [RNA exp1]

ABSTRACT: Deletion of Klotho enhancer deepens sexual dimorphism of gene expression without impacting female resistance to kidney injury [RNA exp1]

PROVIDER: PRJNA1020778 | ENA |

REPOSITORIES: ENA

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Deletion of Klotho enhancer deepens sexual dimorphism of gene expression without impacting female resistance to kidney injury [RNA exp1]

Project description:Sexual dimorphism in kidney injury markers, such as Klotho, is frequently underestimated or disregarded, as most of the preclinical research is done in male animals. Klotho is well-linked to renal health and its deletion in mice results in a severe accelerated aging-like phenotype and premature death. Here, we identified candidate Klotho enhancers and discovered their function using mice carrying deletions in the enhancer loci. Candidate Klotho enhancers were deleted using CRISPR/Cas9 genome editing. Warm ischemia-reperfusion surgery (IRI) was performed bilaterally to induce acute kidney injury and unilaterally in a fibrosis model. Using ChIP-seq and RNA-seq, we analyzed renal chromatin features and gene expression. ELISA and colorimetric assays were used to measure serum FGF23 and serum component levels. Removal of the enhancer caused more substantial reduction in Klotho mRNA levels in female mice compared to males (90 vs. 50%), supported by gene promoter marks remaining more pronounced in males. Weight, lifespan, and fertility of mice lacking the enhancers were not impacted. Only male mutant mice displayed higher Havcr1 expression after IRI than controls (mean 1048 vs. 231.4, p=0.0016). 28 days after unilateral IRI, only males displayed increased fibrosis markers, but with no difference between genotypes. Our findings reveal sexual dimorphism of Klotho gene expression and its enhancer regulation. Only male mutant mice were more susceptible to acute injury and the enhancer deletion had no impact on fibrosis. Additional investigation into the mechanisms governing Klotho regulation is imperative to reassess its effectiveness as a kidney injury marker.

2024-04-04 | GSE243945 | GEO

Deletion of Klotho enhancer deepens sexual dimorphism of gene expression without impacting female resistance to kidney injury [ChIP]

2024-04-04 | GSE243944 | GEO

Deletion of Klotho enhancer deepens sexual dimorphism of gene expression without impacting female resistance to kidney injury [RNA exp2]

2024-04-04 | GSE255885 | GEO

Deletion of Klotho enhancer deepens sexual dimorphism of gene expression without impacting female resistance to kidney injury

Project description:Deletion of Klotho enhancer deepens sexual dimorphism of gene expression without impacting female resistance to kidney injury

| PRJNA1020768 | ENA

Deletion of Klotho enhancer deepens sexual dimorphism of gene expression without impacting female resistance to kidney injury [ChIP]

Project description:Deletion of Klotho enhancer deepens sexual dimorphism of gene expression without impacting female resistance to kidney injury [ChIP]

| PRJNA1020775 | ENA

Deletion of Klotho enhancer deepens sexual dimorphism of gene expression without impacting female resistance to kidney injury [RNA exp2]

Project description:Deletion of Klotho enhancer deepens sexual dimorphism of gene expression without impacting female resistance to kidney injury [RNA exp2]

| PRJNA1076918 | ENA

Deletion of Klotho enhancer deepens sexual dimorphism of gene expression without impacting female resistance to kidney injury

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

2024-04-04 | GSE243946 | GEO

Sexual dimorphism in mice

Project description:Sexual dimorphism in mice

| PRJEB2572 | ENA

Sexual dimorphism in osteogenic differentiation

Project description:Sexual dimorphism in osteogenic differentiation

| PRJNA768873 | ENA

Extrarenal α-klotho expression in human tissues

Project description:α-Klotho has emerged as a powerful regulator of the ageing process. To-date, the expression profile of α-Klotho in human tissues is unknown and its existence in some human tissue types is subject to much controversy. Objective: This is the first study to characterize system-wide tissue expression of transmembrane α-Klotho in humans. We have employed next generation targeted proteomic analysis using Parallel Reaction Monitoring (PRM) in parallel with conventional antibody-based methods to determine the expression and spatial distribution of human α-Klotho expression in health. Results: The distribution of α-Klotho in human tissues from various organ systems, including arterial, epithelial, endocrine, reproductive and neuronal tissues was first identified by immunohistochemistry. Kidney tissues showed strong α-Klotho expression, while liver did not reveal a detectable signal. These results were next confirmed by western blotting of both whole tissues and primary cells. To validate our antibody-based results, α-Klotho expressing tissues were subjected to PRM mass spectrometry identifying peptides specific for the full length, transmembrane α-Klotho isoform. Conclusions: The data presented confirms α-Klotho expression in the kidney tubule and in artery, and provides evidence of α-Klotho expression across organ systems and cell-types that have not previously been described in humans.

2015-10-13 | PXD002775 | Pride

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