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Comprehensive Expression Analysis of mRNA and microRNA for Investigation of Compensatory Mechanisms in the Rat Kidney after Unilateral Nephrectomy

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE144264 | GEO | 2020/04/01

REPOSITORIES: GEO

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Comprehensive Expression Analysis of mRNA and microRNA for Investigation of Compensatory Mechanisms in the Rat Kidney after Unilateral Nephrectomy (Male_mRNA)

Project description:Compensation is a physiological response that occurs during chemical exposure to maintain homeostasis. Because compensatory responses are not usually considered adverse effects, it is important to understand compensatory mechanisms for chemical risk assessment. Although the kidney is a major target organ for toxicity, there is controversy over whether hyperplasia or hypertrophy contributes to the compensatory mechanism, and there is limited information to apply for chemical risk assessment. In the current study, compensatory mechanisms of the kidney were investigated in a unilateral nephrectomy (UNx) model using adult male and female rats. In residual kidneys of male and female rats after UNx, 5-bromo-2'-deoxyuridine-labeling indices and mRNA expression of cell cycle-related genes were increased, although there were no fluctuations in mRNA expression of transforming growth factor-β1, which contributes to hypertrophy in renal tubules. Pathway analysis using mRNA expression data from a cDNA microarray revealed that canonical pathways related to cell proliferation were mainly activated and that forkhead box M1 (FOXM1) was an upstream regulator of compensatory cell proliferation in residual kidneys of male and female rats. cDNA microarray for microRNAs (miRNAs) demonstrated that 9 miRNAs were downregulated in residual kidneys, and mRNA/miRNA integrated analysis indicated that miRNAs were associated with the expression of factors downstream of FOXM1. Overall, these results suggested that FOXM1-mediated hyperplasia rather than hypertrophy contributed to compensatory mechanisms in the kidney and that miRNAs regulated downstream FOXM1 signaling. These results will be beneficial for evaluating nephrotoxicity in chemical risk assessment and for developing new biomarkers to predict nephrotoxicity.

2020-04-01 | GSE144262 | GEO

Comprehensive Expression Analysis of mRNA and microRNA for Investigation of Compensatory Mechanisms in the Rat Kidney after Unilateral Nephrectomy (Male_miRNA)

2020-04-01 | GSE144261 | GEO

Comprehensive Expression Analysis of mRNA and microRNA for Investigation of Compensatory Mechanisms in the Rat Kidney after Unilateral Nephrectomy (Female_mRNA)

2020-04-01 | GSE144263 | GEO

Comprehensive Expression Analysis of mRNA and microRNA for Investigation of Compensatory Mechanisms in the Rat Kidney after Unilateral Nephrectomy

Project description:Comprehensive Expression Analysis of mRNA and microRNA for Investigation of Compensatory Mechanisms in the Rat Kidney after Unilateral Nephrectomy

| PRJNA603235 | ENA

Comprehensive Expression Analysis of mRNA and microRNA for Investigation of Compensatory Mechanisms in the Rat Kidney after Unilateral Nephrectomy (Male_miRNA)

Project description:Comprehensive Expression Analysis of mRNA and microRNA for Investigation of Compensatory Mechanisms in the Rat Kidney after Unilateral Nephrectomy (Male_miRNA)

| PRJNA603239 | ENA

Comprehensive Expression Analysis of mRNA and microRNA for Investigation of Compensatory Mechanisms in the Rat Kidney after Unilateral Nephrectomy (Male_mRNA)

Project description:Comprehensive Expression Analysis of mRNA and microRNA for Investigation of Compensatory Mechanisms in the Rat Kidney after Unilateral Nephrectomy (Male_mRNA)

| PRJNA603238 | ENA

Comprehensive Expression Analysis of mRNA and microRNA for Investigation of Compensatory Mechanisms in the Rat Kidney after Unilateral Nephrectomy (Female_mRNA)

Project description:Comprehensive Expression Analysis of mRNA and microRNA for Investigation of Compensatory Mechanisms in the Rat Kidney after Unilateral Nephrectomy (Female_mRNA)

| PRJNA603237 | ENA

Immune cells and compensatory renal hypertrophy after unilateral nephrectomy

Project description:Background: The underlying mechanisms of compensatory renal hypertrophy (CRH) after unilateral nephrectomy (UNX) are complex and incompletely understood. Most studies have examined hemodynamic and tubular epithelial factors. We studied immune cells in CRH after UNx in mice. Methods: Following UNx of the left kidney of C57BL/6J WT mice, GFR measurements, flow cytometry, single-cell RNA sequencing, and measurements of remnant kidney were performed over 8-weeks period. Rag1-/- mice lacking T and B cells were studied to begin to study the role of direct role of adaptive immune cells in CRH. Results: The largest increase in GFR and increase in kidney weight-to-body weight ratio (KW:BW) in WT mice was at 24 hours, after which GFR remained relatively constant while KW:BW steadily increased. Immune cell populations exhibited dynamic and time-dependent fluctuations following UNx. Early responses (4 and 72 hours) were characterized by significant changes in CD4+ T cells, CD8+ T cells, macrophages, neutrophils, and dendritic cells. Later time points (1 to 8 weeks) showed increased effector memory T cells and B cells, with decline in naïve T cells and macrophages. GFR was significantly higher at 1 week and 4 weeks in Rag1-/- mice compared to controls. Conclusions: Immune cells undergo significant changes in numbers, phenotype and transcriptional programming during CRH after UNx, and could have a direct role in modifying GFR adaptations.

2025-06-30 | GSE300404 | GEO