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Single cell RNA-seq analyses of kidney repair and how maladaptive repair leads to kidney atrophy following ischemia/reperfusion injury

ABSTRACT: Single cell RNA-seq analyses of kidney repair and how maladaptive repair leads to kidney atrophy following ischemia/reperfusion injury

PROVIDER: PRJNA679306 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13081929.fastq.gz	Fastqsanger.gz
	SRR13081930.fastq.gz	Fastqsanger.gz
	SRR13081931.fastq.gz	Fastqsanger.gz
	SRR13081932.fastq.gz	Fastqsanger.gz

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Single cell RNA-seq analyses of kidney repair and how maladaptive repair leads to kidney atrophy following ischemia/reperfusion injury

Project description:To better understand the pathogenesis of AKI-to-CKD transition and specifically the mechanism of kidney atrophy, we compared the kidney response to an identical time of ischemic injury between mice subjected to unilateral ischemia/reperfusion (U-IRI) to induce atrophy and those subjected to unilateral IRI with contralateral nephrectomy (IRI/CL-NX) to induce adaptive repair. We performed single cell RNA-sequencing (scRNA-seq) analyses on day 14 after injury to identify major cell types in the kidney and the differential transcriptional response between the models in each cell type.

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Immune-mediated Tubule Atrophy Promotes Acute Kidney Injury to Chronic Kidney Disease Transition

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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.

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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.

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Project description:Recently, acute kidney injury (AKI) is thought to develop a predisposition toward chronic kidney disease. But the detailed mechanism of the disease progression after AKI is unknown. We made two ischemia-reperfusion injury (IRI) mice models, repaired kidney model and atrophic kidney model, and studied the mechanism that kidney after IRI became atrophy. We found that the atrophy kidney model had two peaks of apoptosis 3 and 14 days after IRI, whereas the repaired kidney model had only one apoptosis peak 3 days after IRI. We showed that the second apoptosis is responsible for the kidney atrophy. Moreover, apoptotic ligands, TNFα and FasL were upregulated at the same time of two apoptosis peaks on the atrophic kidney, and blockade of them before IRI prevented kidney from falling into atrophy. Surprisingly, inhibition of the second apoptosis by anti-TNFα antibody protected from renal atrophy. We propose that apoptosis might play a major role in AKI progression and blockade of TNFα after IRI will be a new therapeutic approach for AKI.

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Project description:Ischemia/reperfusion (I/R) leads to Acute Kidney Injury. HIF-1? is a key factor during organ response to I/R. We previously demonstrated that HIF-1? is induced during renal reperfusion, after ischemia. Here we investigate the role of HIF-1? and the HIF-1? dependent mechanisms in renal repair after ischemia. By interference of HIF-1? in a rat model of renal I/R, we observed loss of expression and mis-localization of e-cadherin and induction of ?-SMA, MMP-13, TGF?, and collagen I. Moreover, we demonstrate that HIF-1? inhibition promotes renal cell infiltrates by inducing IL-1?, TNF-?, MCP-1 and VCAM-1, through NFkB activity. In addition, HIF-1? inhibition induced proximal tubule cells proliferation but it did not induce compensatory apoptosis, both in vivo. In vitro, HIF-1? knockdown in HK2 cells subjected to hypoxia/reoxygenation (H/R) promote cell entry into S phase, correlating with in vivo data. HIF-1? interference leads to downregulation of miR-127-3p and induction of its target gene Bcl6 in vivo. Moreover, modulation of miR-127-3p in HK2 cells subjected to H/R results in EMT regulation: miR127-3p inhibition promote loss of e-cadherin and induction of ?-SMA and collagen I. In conclusion, HIF-1? induction during reperfusion is a protector mechanism implicated in a normal renal tissue repair after I/R.

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Project description:The kidney tubules have tremendous capacity to repair after acute injury, however, pathways guiding adaptive and maladaptive (fibrotic) repair are poorly understood. We developed a model of adaptive and maladaptive kidney regeneration by titrating ischemic injury dose. We performed detailed biochemical and histological analysis and profiled transcriptomic changes at bulk and single-cell level in >110,000 cells over time. Our analysis highlighted kidney proximal tubule (PT) cells as key susceptible cells to injury. Adaptive PT repair correlated with fatty acid oxidation and oxidative phosphorylation. We identified a specific maladaptive/profibrotic PT cluster after long ischemia. These cells expressed proinflammatory and profibrotic cytokines and myeloid cell chemotactic factor. Druggability analysis highlighted pyroptosis and ferroptosis as vulnerable pathways in these profibrotic cells. Pharmacological targeting of pyroptosis/ferroptosis in animal model, pushed cells towards adaptive repair and successfully reduced fibrosis. In summary, our single-cell analysis defined key differences in adaptive and maladaptive repair and identified druggable pathways for pharmacological intervention to prevent kidney fibrosis.

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