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Links from GEO DataSets

Items: 20

1.

The Role of SOX9 in hypoxia/reoxygenation (H/R) injuried mice primary renal tubular epithelial cells

(Submitter supplied) The Role of SOX9 in hypoxia/reoxygenation (H/R) injuried mice primary renal tubular epithelial cells Purpose: we performed comparative RNA-seq analyses to identify differentially expressed genes between Knockdown of Sox9 and negtive control in hypoxia/reoxygenation (H/R) injuried mice primary renal tubular epithelial cells. Methods:we grew mouse primary renal tubular epithelial cells to approximately 50% confluence, transfected using EndoFectin™ Max (GeneCopoeia, China) 12h before suffering to H/R injury. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
6 Samples
Download data: CSV
Series
Accession:
GSE174811
ID:
200174811
2.

Transient upregulation of EGR1 signaling enhances kidney repair by activating SOX9+ renal tubular cells

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
15 Samples
Download data
Series
Accession:
GSE174812
ID:
200174812
3.

The Role of EGR1 in hypoxia/reoxygenation (H/R) injuried mice primary renal tubular epithelial cells

(Submitter supplied) The Role of EGR1 in hypoxia/reoxygenation (H/R) injuried mice primary renal tubular epithelial cells Purpose: we performed comparative RNA-seq analyses to identify differentially expressed genes between Knockdown of Egr1 and negtive control in hypoxia/reoxygenation (H/R) injuried mice primary renal tubular epithelial cells. Methods:we grew mouse primary renal tubular epithelial cells to approximately 50% confluence, transfected using EndoFectin™ Max (GeneCopoeia, China). more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
9 Samples
Download data: CSV
Series
Accession:
GSE174808
ID:
200174808
4.

SOX9 promotes stress-responsive transcription of VGF nerve growth factor inducible gene in renal tubular epithelial cells 

(Submitter supplied) Acute kidney injury (AKI) is a common clinical condition associated with diverse etiologies and abrupt loss of renal function. In patients with sepsis, rhabdomyolysis, cancer, as well as cardiovascular disorders, the underlying disease or associated therapeutic interventions can cause hypoxic, cytotoxic, and inflammatory insults to renal tubular epithelial cells (RTECs) resulting in the onset of AKI. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
20 Samples
Download data: TXT
Series
Accession:
GSE153625
ID:
200153625
5.

Identification of LncRNAs and mRNAs involved in renal ishchemia reperfusion injury

(Submitter supplied) The identification of the expression patterns of long non‑coding RNAs (lncRNAs) and mRNAs in the kidney under normal and renal ischemia/reperfusion (IR) conditions is essential for understanding the genetic mechanisms underlying the pathogenesis of renal IR injury. Here, we have carried out a genome-wide long non-coding RNA and mRNA microarray analysis in mice kidneys with IR. The data revealed that the expression profiles of lncRNAs and mRNAs in the kidneys differed markedly between the Sham group and IR group, and in total 276 differentially expressed (>2‑fold) lncRNAs (201 upregulated, 75 downregulated) and 267 mRNAs (192 upregulated, 75 downregulated) were identified. more...
Organism:
Mus musculus
Type:
Expression profiling by array; Non-coding RNA profiling by array
Platform:
GPL25454
6 Samples
Download data: TXT
Series
Accession:
GSE131454
ID:
200131454
6.

WT1+ parietal epithelial progenitor cells are essential for renal proximal tubule repair and regeneration

(Submitter supplied) Purpose: We have found that WT1+ parietal epithelial progenitor cells contribute to renal proximal tubule repair and regeneration by cell lineage tracing and direct differentiation analysis, but the transcription profile of these WT1+ PECs is largely unkown. Here, we aimed to unveil the transcriptional features of WT1+ PECs through single-cell RNA sequencing (scRNA-seq). Methods: Single cell suspension was prepared from kidney cortex of WT1CreERT2; Rosa26-tdTfl/+ mice that underwent sham or ischemic reperfusion injury (IRI) 24h .TdT+ cells were enriched by fluorescence activated cell sorter (FACS) and further analyzed with BD Rhapsody platform. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
3 Samples
Download data: TSV, TXT
Series
Accession:
GSE184601
ID:
200184601
7.

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

(Submitter supplied) 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. more...
Organism:
Rattus norvegicus
Type:
Expression profiling by array
Platform:
GPL14746
12 Samples
Download data: TXT
Series
Accession:
GSE148420
ID:
200148420
8.

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

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL19057 GPL24247
41 Samples
Download data: BIGWIG, H5, NARROWPEAK, TBI, TSV
Series
Accession:
GSE249781
ID:
200249781
9.

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

(Submitter supplied) 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. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24247
2 Samples
Download data: H5, TBI, TSV
Series
Accession:
GSE249780
ID:
200249780
10.

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

(Submitter supplied) 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. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
9 Samples
Download data: CSV
Series
Accession:
GSE249778
ID:
200249778
11.

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

(Submitter supplied) 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. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
6 Samples
Download data: CSV
Series
Accession:
GSE249777
ID:
200249777
12.

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

(Submitter supplied) 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. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
24 Samples
Download data: BIGWIG, NARROWPEAK
Series
Accession:
GSE249776
ID:
200249776
13.

Injured Mouse Kidney

(Submitter supplied) Mouse kidneys were harvested at either 48 hours or 10 days post injury and subjected to single-cell RNA sequencing
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
5 Samples
Download data: CSV, MTX, TSV
Series
Accession:
GSE196929
ID:
200196929
14.

The injury-induced transcription factor SOX9 alters the expression of LBR, HMGA2, and HIPK3 in human kidney

(Submitter supplied) Induction of SRY box transcription factor 9 (SOX9) has been shown to occur in response to kidney injury in rodents, where SOX9-positive cells proliferate and regenerate the proximal tubules of injured kidneys. Additionally, SOX9-positive cells demonstrate a capacity to differentiate toward other nephron segments. Here, we characterized the role of SOX9 in normal and injured human kidneys. SOX9 expression was found to colocalize with a proportion of so-called scattered tubular cells in the uninjured kidney, a cell population previously shown to be involved in kidney injury and regeneration. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
9 Samples
Download data: TXT
Series
Accession:
GSE207594
ID:
200207594
15.

Transcriptome profile of a murine renal bilateral ischemia reperfusion model 2 hours to 12 months post injury

(Submitter supplied) Acute kidney injury (AKI) is associated with an increased risk of chronic kidney disease (CKD). To extend our understanding of renal repair, and its limits, we performed a detailed molecular characterization of a murine ischemia reperfusion injury (IRI) model for 12 months post injury. RNA-seq analysis highlights a cascade of temporal specific gene expression patterns related to tubular injury/repair, fibrosis, innate and adaptive immunity.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL19057 GPL13112
49 Samples
Download data: XLSX
Series
Accession:
GSE98622
ID:
200098622
16.

Single-cell RNA sequencing identifies response of renal lymphatic endothelial cells to acute kidney injury

(Submitter supplied) Background: The inflammatory response to acute kidney injury (AKI) likely dictates future renal health. Lymphatic vessels are responsible for maintaining tissue homeostasis through transport and immunomodulatory roles. Due to the relative sparsity of lymphatic endothelial cells (LECs) in the kidney, past sequencing efforts have not characterized these cells and their response to AKI. Methods: Here we characterized murine renal LEC subpopulations by single-cell RNA sequencing and investigated their changes in cisplatin AKI 72 hours post injury. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
2 Samples
Download data: MTX, TSV
Series
Accession:
GSE236199
ID:
200236199
17.

Complement induced aberrant epigenetic modifications in renal tubular epithelial cells and accelerates senescence after kidney transplantation by Wnt pathway

(Submitter supplied) Epigenetic mechanisms as DNA methylation can affect allograft outcome after kidney transplantation, accelerating renal aging. Complement system is the major player of ischemia reperfusion (I/R) injury and Renal Proximal Tubular Cells (RPTEC) are known to express C5a receptor (C5aR). However, little is known about the downstream effect of C5a-C5aR interaction. We performed a whole-genome DNA methylation analysis on C5a stimulated RPTEC and found several regions regulating genes involved in cell cycle control, DNA damage checkpoints and WNT signaling. more...
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL13534
6 Samples
Download data: TXT
Series
Accession:
GSE115227
ID:
200115227
18.

Gpr97 exacerbates AKI via mediating Sema3A signaling

(Submitter supplied) We have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to distinguish between the mice with renal IRI injury and sham-operated group.Expression of Gpr97 from this signature was quantified in the same kind of samples by real-time PCR, confirming the change pattern. By microarray analysis, we found that IR-induced Sema3A expression was significantly abolished by Gpr97 deficiency in mice
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL7202
6 Samples
Download data: TXT
Series
Accession:
GSE108195
ID:
200108195
19.

Enhancer Regulation in Kidney Repair [RNA-Seq 2]

(Submitter supplied) The endogenous repair process of the mammalian kidney allows rapid recovery after acute kidney injury (AKI) through robust proliferation of tubular epithelial cells. There is currently limited understanding of which transcriptional regulators activate these repair programs and how transcriptional deregulation leads to maladaptive repair. Here we investigate the existence of enhancer dynamics in the regenerating mouse kidney.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21493
8 Samples
Download data: TXT
Series
Accession:
GSE125056
ID:
200125056
20.

Enhancer Regulation in Kidney Repair

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL21493 GPL17021
36 Samples
Download data: BEDGRAPH, TXT
Series
Accession:
GSE114294
ID:
200114294
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