The role of cadherin-11 in Unx/AngII induced kidney injury [Huffstater_Unx]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA784131 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The role of cadherin-11 in Unx/AngII induced kidney injury
| PRJNA784130 | ENA
Project description:The role of cadherin-11 in Unx/AngII induced kidney injury [Huffstater_AA]
| PRJNA784132 | ENA
Project description:The objective of this study was to understand the impact of losing cadherin-11 (CDH11) on kidney injury. CDH11 has previously been demonstrated to be associated with a number of fibrotic diseases, but its role in kidney injury remains unknown. In vivo models of kidney injury demonstrated improved renal function and reduced tubulointerstitial fibrosis with CDH11 inhibition. However, the mechanism by which CDH11 inhibition mitigates kidney injury is unknown. RNAseq analysis showed altered expression of over 50 genes in two models of kidney injury when CDH11-/- mice were compared with CDH11+/+ mice. These results together indicate that CDH11 deletion alters many genes and pathways that could contribute to kidney injury, including alpha-1 antitrypsin, which is increased in CDH11-/- mice and has been shown to be beneficial in kidney injury.
2024-11-26 | GSE189681 | GEO
Project description:The objective of this study was to understand the impact of losing cadherin-11 (CDH11) on kidney injury. CDH11 has previously been demonstrated to be associated with a number of fibrotic diseases, but its role in kidney injury remains unknown. In vivo models of kidney injury demonstrated improved renal function and reduced tubulointerstitial fibrosis with CDH11 inhibition. However, the mechanism by which CDH11 inhibition mitigates kidney injury is unknown. RNAseq analysis showed altered expression of over 50 genes in two models of kidney injury when CDH11-/- mice were compared with CDH11+/+ mice. These results together indicate that CDH11 deletion alters many genes and pathways that could contribute to kidney injury, including alpha-1 antitrypsin, which is increased in CDH11-/- mice and has been shown to be beneficial in kidney injury.
2024-11-26 | GSE189680 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2024-11-26 | GSE189682 | GEO
Project description:Proteinuria is pathogenic to proximal tubular cells (PTC) and linked with progression to renal failure. Angiotensin II (AngII) is also independently involved in the pathogenesis of progressive renal injury in varied kidney disease. The effects of human serum albumin (HSA) overload, AngII and candesartan, a specific inhibitor of AngII type 1 recptor, on the changes in gene protein expression stimulated by oxidative stress in PTC were assesed using cDNA microarrays. Keywords: stress response Cells were growth arrested for 48 h in serum-free DMEM/Ham's F-12 medium with 5.5 mM glucose, 2 mM L-glutamine,100 U/ml penicillin, 100 ug/ml streptomycin, 20 mM Hepes. Media were refreshed and cells were incubated for 24h in conditioned media alone, or with media supplemented with 30mg/ml of different HSA preparations, 1 uM AngII or AngII in the presence of candesartan. After further 24 h under standard cell culture conditions (37C, 5% CO2) cells were subjected to RNA extraction.
2010-06-25 | E-GEOD-10648 | biostudies-arrayexpress
Project description:Proteinuria is pathogenic to proximal tubular cells (PTC) and linked with progression to renal failure. Angiotensin II (AngII) is also independently involved in the pathogenesis of progressive renal injury in varied kidney disease. The effects of human serum albumin (HSA) overload, AngII and candesartan, a specific inhibitor of AngII type 1 recptor, on the changes in gene protein expression stimulated by oxidative stress in PTC were assesed using cDNA microarrays. Keywords: stress response
2008-02-28 | GSE10648 | GEO
Project description:Cadherin-11 expression is associated with tumor progression and metastasis in various cancers, including basal-like breast carcinoma and advanced prostate cancer, and invasive cell lines, yet is absent in normal epithelium. We now show cadherin-11 attenuation in aggressive breast and prostate cancer cells results in marked decreases in proliferation, migration, and invasion. Cadherin-11 depletion in MDA-231 cells prevents tumor growth in mice and alters gene expression associated with poor prognosis malignancies. Additionally, a novel small molecule inhibitor targeting its unique adhesive interface significantly inhibits the growth and migration of cadherin-11 positive cells. Cadherin-11 is essential for malignant progression of MDA-231 basal-type cells, and may serve as both an aggressive tumor marker and viable therapeutic target for poor prognosis carcinomas expressing it.
2010-02-22 | GSE14943 | GEO
Project description:Microarray analysis of human kidneys with acute kidney injury (AKI) has been limited because such kidneys are seldom biopsied. However, all kidney transplants experience AKI, and early kidney transplants without rejection are an excellent model for human AKI: they are screened to exclude chronic kidney disease, frequently biopsied, and have extensive follow-up. We used histopathology and microarrays to compare indication biopsies from 28 transplants with AKI to 11 pristine protocol biopsies of stable transplants. Kidneys with AKI showed increased expression of 394 injury-repair response associated transcripts, including many known epithelial injury molecules (e.g. ITGB6, LCN2), tissue remodeling molecules (e.g. VCAN), and inflammation molecules (S100A8, ITGB3). Many other genes also predict the phenotype, depending on statistical filtering rules, including AKI biomarkers as HAVCR1 and IL18. Most mouse orthologs of the top injury-repair transcripts were increased in published mouse AKI models. Pathway analysis of the injury-repair transcripts revealed similarities to cancer, development, and cell movement. The injury-repair transcript score AKI kidneys correlated with reduced function, future recovery, brain death, and need for dialysis, but not future graft loss. In contrast, histologic features of "acute tubular injury" did not correlate with function or with the molecular changes. Thus the injury-repair associated transcripts represent a massive coordinate injury-repair response of kidney parenchyma to AKI, similar to mouse AKI models, and provide an objective measure for assessing the severity of AKI in kidney biopsies and validation for the use of many AKI biomarkers. AKI biopsies sample names and CEL files are from GSE21374. All consenting renal transplant patients undergoing biopsies for cause as standard of care between 09/2004 and 10/2007 at the university of Alberta or between 11/2006 and 02/2007 at the University of Illinois were included in the analysis. In addition to the cores required for standard histopathology, we collected one core for gene expression studies. the relationship between gene expression in the biopsy and subsequent graft loss was analyzed. This dataset is part of the TransQST collection.
2012-02-21 | E-GEOD-30718 | biostudies-arrayexpress
Project description:The goal of this observational study is to compare anesthetic modalities (intravenous propofol anesthesia with sevoflurane gas anesthesia) in patients who underwent colorectal cancer resection surgery regarding the outcome of acute kidney injury.
The main questions it aims to answer are:
* is there a difference in acute kidney injury incidence in the two anesthetic modalities?
* is there a difference in plasma creatinine between the two anesthetic modalities?
* are there any patient characteristics or intraoperative factors that effect the incidence of acute kidney injury in either anesthetic modality?
The study will analyze data from the CAN clinical trial database. (Cancer and Anesthesia: Survival After Radical Surgery - a Comparison Between Propofol or Sevoflurane Anesthesia, NCT01975064)
| 2751857 | ecrin-mdr-crc