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Sox9 switch links regeneration to fibrosis at the single-cell level in mammalian kidneys [RNA-Seq 1]

ABSTRACT: Sox9 switch links regeneration to fibrosis at the single-cell level in mammalian kidneys [RNA-Seq 1]

PROVIDER: PRJNA1050314 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27153939_1.fastq.gz	Fastqsanger.gz
	SRR27153939_2.fastq.gz	Fastqsanger.gz
	SRR27153940_1.fastq.gz	Fastqsanger.gz
	SRR27153940_2.fastq.gz	Fastqsanger.gz
	SRR27153941_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Sox9 switch links regeneration to fibrosis at the single-cell level in mammalian kidneys

Project description:Sox9 switch links regeneration to fibrosis at the single-cell level in mammalian kidneys

| PRJNA1050312 | ENA

Sox9 switch links regeneration to fibrosis at the single-cell level in mammalian kidneys [snATAC-Seq]

Project description:Sox9 switch links regeneration to fibrosis at the single-cell level in mammalian kidneys [snATAC-Seq]

| PRJNA1050316 | ENA

Sox9 switch links regeneration to fibrosis at the single-cell level in mammalian kidneys [CUT&Run]

Project description:Sox9 switch links regeneration to fibrosis at the single-cell level in mammalian kidneys [CUT&Run]

| PRJNA1050315 | ENA

Sox9 switch links regeneration to fibrosis at the single-cell level in mammalian kidneys [RNA-Seq 2]

Project description:Sox9 switch links regeneration to fibrosis at the single-cell level in mammalian kidneys [RNA-Seq 2]

| PRJNA1050317 | ENA

Sox9 switch links regeneration to fibrosis at the single-cell level in mammalian kidneys [snATAC-Seq]

Project description:The steps governing healing with or without fibrosis within the same microenvironment are unclear. After acute kidney injury (AKI), the injured proximal tubular epithelial cells activate Sox9 for self-restoration. Using head-to-head comparison of injury- induced Sox9-lineages via spatiotemporal mapping, single-cell sequencing, and single-nuclei chromatin accessibility profiling, we identified a dynamic SOX9 switch. Lineages that regenerated epithelia silenced SOX9 and healed without fibrosis (SOX9on-off). In contrast, lineages that maintained Sox9 activity in attempt to regenerate, demarcated by SOX9-induced Cadherin 6 (SOX9on-on CDH6pos ) cell state, generated single-cell Wnt activity to provoke a fibroproliferative response in adjacent fibroblasts, driving AKI to chronic kidney disease. Transplanted human kidneys displayed similar SOX9/CDH6/WNT2B responses post-injury. Thus, we uncovered a mechanism linking fibrosis to sustained efforts to regenerate the injured tissue.

2024-02-26 | GSE249780 | GEO

Sox9 switch links regeneration to fibrosis at the single-cell level in mammalian kidneys [CUT&Run]

2024-02-26 | GSE249776 | GEO

Sox9 switch links regeneration to fibrosis at the single-cell level in mammalian kidneys [RNA-Seq 2]

2024-02-26 | GSE249778 | GEO

Sox9 switch links regeneration to fibrosis at the single-cell level in mammalian kidneys [RNA-Seq 1]

2024-02-26 | GSE249777 | GEO

SOX9 switch links regeneration to fibrosis at the single-cell level in mammalian kidneys.

Project description:The steps governing healing with or without fibrosis within the same microenvironment are unclear. After acute kidney injury (AKI), injured proximal tubular epithelial cells activate SOX9 for self-restoration. Using a multimodal approach for a head-to-head comparison of injury-induced SOX9 lineages, we identified a dynamic SOX9 switch in repairing epithelia. Lineages that regenerated epithelia silenced SOX9 and healed without fibrosis (SOX9on-off). By contrast, lineages with unrestored apicobasal polarity maintained SOX9 activity in sustained efforts to regenerate, which were identified as a SOX9on-on Cadherin6pos cell state. These reprogrammed cells generated substantial single-cell WNT activity to provoke a fibroproliferative response in adjacent fibroblasts, driving AKI to chronic kidney disease. Transplanted human kidneys displayed similar SOX9/CDH6/WNT2B responses. Thus, we have uncovered a sensor of epithelial repair status, the activity of which determines regeneration with or without fibrosis.

| S-EPMC11345873 | biostudies-literature

Sox9 controls self-renewal of oncogene targeted cells and links tumor initiation and invasion [ChIP-Seq]

Project description:Sox9 is a transcription factor expressed in most solid tumors. However, the molecular mechanisms underlying Sox9 function during tumorigenesis remain unclear. Here, using a genetic mouse model of basal cell carcinoma (BCC), the most frequent cancer in human, we show that Sox9 is expressed from the earliest step of tumor formation in a Wnt/β-catenin dependent manner. Deletion of Sox9 together with the constitutive activation of Hedgehog (HH) signaling completely prevents BCC formation and leads to a progressive loss of oncogene expressing cells. Transcriptional profiling of oncogene expressing cells with Sox9 deletion, combined with in vivo ChIP-sequencing uncovers a cancer-specific gene network regulated by Sox9 that promotes stemness, extracellular matrix (ECM) deposition and cytoskeleton remodeling while repressing epidermal differentiation. Our study identifies the molecular mechanisms regulated by Sox9 that links tumor initiation and invasion. Sox9 ChIP-seq analysis in K14CreER SmoM2 cells.

2015-05-13 | E-GEOD-68755 | biostudies-arrayexpress

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