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Glucocorticoids induce a maladaptive epithelial stress response to aggravate acute kidney injury [RNA]

ABSTRACT: Glucocorticoids induce a maladaptive epithelial stress response to aggravate acute kidney injury [RNA]

PROVIDER: PRJNA1154560 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30484335.fastq.gz	Fastqsanger.gz
	SRR30484336.fastq.gz	Fastqsanger.gz
	SRR30484337.fastq.gz	Fastqsanger.gz
	SRR30484338.fastq.gz	Fastqsanger.gz
	SRR30484339.fastq.gz	Fastqsanger.gz

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Glucocorticoids induce a maladaptive epithelial stress response to aggravate acute kidney injury

Project description:Glucocorticoids induce a maladaptive epithelial stress response to aggravate acute kidney injury

| PRJNA1154554 | ENA

Glucocorticoids induce a maladaptive epithelial stress response to aggravate acute kidney injury [ATAC]

Project description:Glucocorticoids induce a maladaptive epithelial stress response to aggravate acute kidney injury [ATAC]

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Glucocorticoids induce a maladaptive epithelial stress response to aggravate acute kidney injury [ATAC]

Project description:Acute kidney injury (AKI) is a frequent and challenging clinical condition associated with high morbidity and mortality. In AKI, renal tubular epithelial cells (TECs) are a primary site of damage, and recovery from AKI depends on TEC plasticity. However, the molecular mechanisms underlying adaptation and maladaptation of TECs in AKI remain largely unclear. Here, our analyses of mouse kidney tubuloids showed that TEC injury resulted in activation of the glucocortiocoid receptor by endogenous glucocorticoids, which aggravated tubular damage. The detrimental effect of endogenous glucocorticoids on injured TECs was exacerbated by the administration of the widely clinically used synthetic glucocorticoid, dexamethasone, as indicated by experiments in mouse kidney tubuloids. Mechanistically, studies in mouse tubuloids demonstrated that glucocorticoid receptor signaling in injured TECs orchestrated a maladaptive transcriptional program to hinder DNA repair and to amplify injury-induced DNA double-strand break formation, as well as to dampen mTOR activity and mitochondrial bioenergetics. This study identifies glucocortiocoid receptor activation as a mechanism of epithelial maladaptation, which is functionally important for acute kidney injury.

2024-09-14 | GSE276041 | GEO

Glucocorticoids induce a maladaptive epithelial stress response to aggravate acute kidney injury [RNA]

2024-09-14 | GSE276040 | GEO

Glucocorticoids induce a maladaptive epithelial stress response to aggravate acute kidney injury

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

2024-09-14 | GSE276043 | GEO

Hypoxic injury triggers maladaptive repair in human kidney organoids [scRNA-seq]

Project description:Reduction in blood supply to the kidneys occurs to certain extent during acute kidney injury (AKI). Individuals who suffered AKI are at risk of developing chronic kidney disease (CKD) through a maladaptive repair process. Currently, the lack of a reliable research model that allows the characterization of the maladaptive regeneration during such transition, impedes the development of effective therapies. Here, we present the first human kidney organoid model that physiologically and morphologically resembles the AKI and the maladaptive regeneration. Kidney organoids were generated from human induced pluripotent stem cells. After 18 days of grow the organoids were under hypoxic conditions for 2 days to simulate AKI. Organoids were collected at day 20 to assess hypoxic injury, and after a 5-day recovery in normoxic conditions to assess maladaptive repair. The transcriptome, proteome and metabolome were profiled. Gene expression analysis of day 20 hypoxic organoids identified signatures of injury, cell death (necroptosis and ferroptosis), cell cycle arrest and changes in metabolism. The maladaptive repair phenotype was supported by enrichment of pathways associated with inflammatory signals, oxidative stress, and tissue remodelling. Specific genes associated with kidney injury and disease such as GDF15, MMP7, ICAM1, TGFB1, CCN1, C3 and S100A8/9 were upregulated. Single-cell RNA sequencing localized expression of maladaptive repair genes and activation of TNF and JAK-STAT signalling pathways specific to tubular epithelial cells. Dysregulation in metabolic pathways such as glycolysis and gluconeogenesis, amino acid and lipid metabolisms were conserved in this model. Altogether, these results support the use of kidney organoids as a model of AKI and early CKD that can be used for biomarker validation, elucidation of pathological mechanisms, and drug screening.

2025-08-15 | GSE242425 | GEO

Hypoxic injury triggers maladaptive repair in human kidney organoids

Project description:Hypoxic injury triggers maladaptive repair in human kidney organoids

| PRJNA1013401 | ENA

Hypoxic injury triggers maladaptive repair in human kidney organoids [scRNA-seq]

Project description:Hypoxic injury triggers maladaptive repair in human kidney organoids [scRNA-seq]

| PRJNA1013406 | ENA

Lineage tracing and single nuclear multiomics reveal novel features of adaptive and maladaptive repair after acute kidney injury

Project description:We combined lineage tracing of cycling (Ki67+) cells with single nuclear multiomics (single nucleus RNA-seq + single nucleus ATAC-seq) to characterize the long-term (4 weeks and 6 months) outcome of cells that initiate proliferation early after acute kidney injury (AKI). The data document a broad proliferative response to injury in epithelial and non-epithelial kidney cell types, identify novel transcription factors governing the adaptive and maladaptive proximal tubule cell state and highlight the importance of enhancer dynamics in determining cell states. Comparison of lineage traced with control proximal tubule cells reveals long-term effects of AKI on proximal tubule cells, even following adaptive repair.

2022-11-22 | GSE209610 | GEO

Immunohistochemical Investigation for Renal Tubules in Adaptive and Maladaptive Repair Process after Renal Tubular Injury in the Kidney of Rats

Project description:Acute kidney injury (AKI) have been thought to be reversible condition, however, emerging evidence demonstrated association between AKI and subsequent development of irreversible fibrosis and chronic kidney disease. In the present study, since recovery of AKI depends on renal tubular regeneration, factors expressing in renal tubules in adaptive or maladaptive repair process were investigated to predict reversibility of kidney injury. In the kidney of female F344 rats subjected to ischemia/reperfusion (I/R), regenerative tubules and dilated tubules were observed at 3 and 7 days after I/R. In fibrotic areas of the kidney of male SD rats subjected to I/R, renal tubules were dilated or atrophied. From microarray data of regenerative tubules, survivin, sex-determining region Y (SRY)-box 9 (SOX9), and CD44 were extracted as factors possibly relating to tubular regeneration or fibrosis. Immunohistochmical analysis demonstrated that survivin and SOX9 expressed in regenerative tubules, while SOX9 also expressed in renal tubules in fibrotic area, indicating that survivin and SOX9 contribute renal tubular regeneration, but sustained SOX9 expression may lead fibrosis. CD44 expressed in dilated tubules at day 3 and 7, and tubules in fibrotic area, suggesting that CD44 expressed in maladaptive tubules. These information will be helpful to consider reversibility of kidney injury.

2020-06-01 | GSE148420 | GEO

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