Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A lack of secretory leukocyte protease inhibitor (SLPI) causes defects in granulocytic differentiation.

ABSTRACT: Expression data from CD34+ hematopoietic cells transduced with control or anti-SLPI shRNA, serum starved and treated with G-CSF.

ORGANISM(S): Homo sapiens

PROVIDER: GSE53353 | GEO | 2014/03/04

SECONDARY ACCESSION(S): PRJNA231777

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

A lack of secretory leukocyte protease inhibitor (SLPI) causes defects in granulocytic differentiation.

Project description:Expression data from CD34+ hematopoietic cells transduced with control or anti-SLPI shRNA, serum starved and treated with G-CSF. CD34+ hematopoietic cells were isolated from the bone marrow of healthy individuals, transduced with lenitvirus-based RFP-expressed shRNA constructs targeting SLPI mRNA or scrambled control shRNA. After 3 days of the transductions, RFP+ cells were sorted, serum starved for 24 hours and treated with G-CSF 10 ng/ml for 18 hours. Total RNA of sorted cells was isolated and used for Affymetrix Exome arrays.

2014-03-04 | E-GEOD-53353 | biostudies-arrayexpress

Secretory Leukocyte Peptidase Inhibitor (SLPI) is a Novel Predictor of Tubulointerstitial Injury and Renal Outcome in Patients with Diabetic Nephropathy

Project description:Tubulointerstitial injury plays an important role in diabetic nephropathy (DN) progression; however, no reliable urinary molecule has been used to predict tubulointerstitial injury and renal outcome of DN clinically. In this study, based on tubulointerstitial transcriptome, we identified secretory leukocyte peptidase inhibitor (SLPI) as the molecule associated with renal fibrosis and prognosis of DN. In tubular cells, high glucose could upregulate SLPI, which bound with β-catenin and GSK-3β reciprocally, abolished the interaction between β-catenin and GSK-3β, diminished GSK-3β-regulated β-catenin phosphorylation and the subsequent ubiquitination and degradation, thus led to β-catenin signaling activation and renal fibrosis. Db/db mice injected with adenovirus carrying Slpi-3xflag-GFP (Ad-Slpi-GFP) developed β-catenin signaling activation in the proximal tubule, worse albuminuria and tubulointerstitial fibrosis. Conversely, Slpi knockout (KO) mice with STZ-induced DN developed less albuminuria, tubulointerstitial fibrosis and β-catenin signaling activation. Furthermore, clinical studies showed that urinary SLPI protein level (uSLPI/Cr) had significant correlation with intrarenal SLPI mRNA and interstitial fibrosis. In an independent prospective cohort enrolled 711 patients with biopsy proven DN, uSLPI/Cr level was significantly associated with eGFR slope and improved the prediction value of renal outcome. Together, our study identified SLPI as a novel critical regulator for the progression of tubulointerstitial injury, which may be used as an independent risk predictor of DN progression.

2022-08-03 | GSE158230 | GEO