Gene expression profile for NGAL overexpression in esophageal squamous carcinoma cell
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE57630 | GEO | 2014/05/14
SECONDARY ACCESSION(S): PRJNA247368
REPOSITORIES: GEO
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Project description:Neutrophil gelatinase associated lipocalin (NGAL), also known as oncogene 24p3, uterocalin, siderocalin or lipocalin 2 (Lcn2), is a member of the lipocalin family. Elevated NGAL involves various functions in malignant cells, even sometimes the conclusions were controversial. NGAL inhibits apoptosis in thyroid cancer and decrease invasion and angiogenesis in pancreatic cancer, but it increase proliferation and metastasis in breast and colon cancer. Nonetheless, the molecular functions and mechanisms of NGAL in ESCC are unknown. To address these issues and to identify genes and biological pathways associated with NGAL functions and mechanism, NGAL was overexpressed by pcDNA3.0 plasmid in ESCC cell line EC109 with an empty plasmid as a control, these two cells were applied for mRNA expression profile analyses to find the differentially expressed genes. Plasmids of pcDNA3.0-NGAL and pcDNA3.0 were transfected into ESCC cell line EC109, respectively. Stable transfected cell clones were selected by G418. The overexpression of NGAL protein was confirmed by western blot. Total RNAs from NGAL overexpressed cells and control cells were extracted for Agilent whole genome oligo microarray. A dye flip was performed for duplicate.
2014-05-14 | E-GEOD-57630 | biostudies-arrayexpress
Project description:CD4+ T cells mediate the pathogenesis of ischemic and nephrotoxic acute kidney injury (AKI), as well as acute injury to other organs. However, the underlying mechanisms of CD4+ T cell-mediated pathogenesis are largely unknown. We therefore conducted unbiased RNA-sequencing to discover novel mechanistic pathways of kidney CD4+ T cells post-ischemia compared to normal mouse kidney. Unexpectedly, lipocalin-2 (Lcn2) gene, which encodes neutrophil gelatinase-associated lipocalin (NGAL) had the highest (~60)-fold increase. The NGAL increase in CD4+ T cells during AKI was confirmed at the mRNA level with real-time PCR and at the protein level with ELISA. NGAL is a potential biomarker for the early detection of AKI and has multiple potential biological functions during organ injury. However, the role of NGAL produced by CD4+ T cells has not been investigated. We found that ischemic AKI in NGAL knockout (KO) mice had worse renal outcomes compared to wild type (WT) mice. Adoptive transfer of NGAL-deficient CD4+ T cells from NGAL KO mice into CD4 KO or WT mice led to worse renal function than transfer of WT CD4+ T cells. In vitro simulated ischemia reperfusion showed that NGAL-deficient CD4+ T cells express higher levels of IFN-γ mRNA compared to WT CD4+ T cells. In vitro differentiation of naive CD4+ T cells to Th17, Th1 and Th2 cells led to significant increase in Lcn2 expression. Human kidney CD4+ T cell NGAL also increased significantly post-ischemia. These results demonstrate an important role for CD4+ T cell NGAL as a mechanism by which CD4+ T cells mediate AKI and extend the importance of NGAL in AKI beyond diagnostics.
2019-11-25 | GSE139171 | GEO
Project description:Human Immunodeficiency Virus (HIV) associated nephropathy (HIVAN) is characterized clinically by both nephrosis and by rapidly progressive kidney dysfunction. HIVAN is characterized histologically by both collapsing focal segmental glomerulosclerosis and prominent tubular damage. Neutrophil Gelatinase Associated Lipocalin (NGAL) is known to be rapidly expressed in distal segments of the nephron at the onset of different types of acute kidney injury, but few studies have examined NGAL in chronic kidney disease models. We found that urinary NGAL (uNGAL) was highly expressed by patients with biopsy proven HIVAN, whereas HIV+ patients without HIVAN demonstrated lower levels. uNGAL was also highly expressed in the TgFVB mouse model of HIVAN, which demonstrated NGAL gene expression in dilated, microcystic segments of the nephron. These data show that NGAL is markedly upregulated in the setting of HIVAN, and suggest that uNGAL levels may provide a non-invasive screening test to detect HIVAN related tubular disease. Microarray data revealed that NGAL was one of the most highly upregulated gene the TgFVB mouse.
2009-12-25 | E-GEOD-14221 | biostudies-arrayexpress
Project description:Human Immunodeficiency Virus (HIV) associated nephropathy (HIVAN) is characterized clinically by both nephrosis and by rapidly progressive kidney dysfunction. HIVAN is characterized histologically by both collapsing focal segmental glomerulosclerosis and prominent tubular damage. Neutrophil Gelatinase Associated Lipocalin (NGAL) is known to be rapidly expressed in distal segments of the nephron at the onset of different types of acute kidney injury, but few studies have examined NGAL in chronic kidney disease models. We found that urinary NGAL (uNGAL) was highly expressed by patients with biopsy proven HIVAN, whereas HIV+ patients without HIVAN demonstrated lower levels. uNGAL was also highly expressed in the TgFVB mouse model of HIVAN, which demonstrated NGAL gene expression in dilated, microcystic segments of the nephron. These data show that NGAL is markedly upregulated in the setting of HIVAN, and suggest that uNGAL levels may provide a non-invasive screening test to detect HIVAN related tubular disease.
2009-12-25 | GSE14221 | GEO
Project description:The early events that signal renal dysfunction in presymptomatic heart failure are unclear. To evaluate this, we performed RNA-seq on kidneys from transgenic mice with cardiac-specific overexpression of mutant alpha-B-crystallin, which develop slowly progressive cardiomyopathy. Presymptomatic transgenic mice display an increase in serum creatinine and in urinary neutrophil gelatinase-associated lipocalin (NGAL), but lack chronic interstitial fibrosis. Presymptomatic transgenic mouse kidneys exhibited a worsened response to ischemia-reperfusion injury based on serum creatinine, urine NGAL, tubule dilation and cast score, and apoptosis. Our findings demonstrate functional renal impairment, urinary biomarker elevations, and gene expression changes that occur in early presymptomatic heart failure, which dramatically increase the susceptibility to subsequent acute kidney injury.
2018-02-16 | GSE99703 | GEO
Project description:During kidney development segmented epithelia of the nephron derive from progenitor cells in the metanephric mesenchyme after induction by secreted molecules from the ureteric bud. We have identified three distinct inductive activities from a ureteric bud cell line. These include leukemia inhibitory factor (LIF), neutrophil gelatinase-associated lipocalin (NGAL) and an active fraction currently referred to as ANX. Each of these activities induces segmented nephron epithelia in isolated rat metanephric mesenchyme over a time period of 7 days. This study was designed to characterize the temporal sequence of gene expression in the course of the conversion process induced by each of the distinct inducers. Experiment Overall Design: Metanephric mesenchymes were microdissected from rat E13.5 embryos. Mesenchymes were cultured on transwells in the presence of either LIF, NGAL or the ANX fraction and RNA was harvested after 1, 2, 3, 4, 5, and 7 days for RNA extraction. Freshly dissected mesenchymes and mesenchymes cultured in the absence of inducers for 1 and 2 days, respectively, served as controls. Each condition was analyzed in duplicate (biological replicates). Biotinylated cRNA was prepared and hybridized to Affymetrix Rat Genome 230 2.0 Microarrays. Expression values were obtained by robust multichip analysis.
2008-06-13 | E-GEOD-5478 | biostudies-arrayexpress
Project description:During kidney development segmented epithelia of the nephron derive from progenitor cells in the metanephric mesenchyme after induction by secreted molecules from the ureteric bud. We have identified three distinct inductive activities from a ureteric bud cell line. These include leukemia inhibitory factor (LIF), neutrophil gelatinase-associated lipocalin (NGAL) and an active fraction currently referred to as ANX. Each of these activities induces segmented nephron epithelia in isolated rat metanephric mesenchyme over a time period of 7 days. This study was designed to characterize the temporal sequence of gene expression in the course of the conversion process induced by each of the distinct inducers. Keywords: time course
2007-07-01 | GSE5478 | GEO
Project description:Transcriptional profiling of mouse primary astrocytes comparing control untreated astrocytes with astrocytes treated with recombinant LCN2 protein (10 micro gram/ml). Goal was to determine the effects of LCN2 treatment on global gene expression in astrocytes. A secreted protein lipocalin-2 (LCN2) has been implicated in diverse cellular processes including cell morphology and migration. We have previously demonstrated that lcn2 mediates reactive astrocytosis. In order to further understand the role of lcn2 in the CNS, astrocyte transcriptome was analyzed following LCN2 treatment. Chemokines were the major group of genes upregulated by LCN2. Two-condition experiment, control untreated astrocytes vs. LCN2 protein treated astrocytes. Biological replicates: 1 control replicates, 1 treated replicates.
2012-06-29 | E-GEOD-15667 | biostudies-arrayexpress
Project description:Lipocalin-2 (LCN2) is a secreted protein involved in innate immunity and also has been associated with several cardiometabolic traits. We examined LCN2 expression in a panel of diverse inbred mouse strains and observed a striking sex difference. Adipose LCN2 was associated with obesity, insulin resistance, dyslipidemia, and hepatic steatosis in females but not males. We expressed LCN2 either in adipose or liver in a tissue specific manner on the background of a whole-body knockout mouse. Adipose LCN2 expression, acting in an autocrine/paracrine manner, promoted metabolic disturbances in females but not males, whereas liver LCN2 expression had no impact on the traits examined. The adipose expression was accompanied by adipose inflammation, fibrosis, and mitochondrial dysfunction, contributing in part to the metabolic disorders. We also show that LCN2 inversely regulates its receptor, LRP2 (or megalin), in a sex-specific manner. Our results demonstrate striking sex- and tissue- specific functions of LCN2.
2018-10-11 | GSE121098 | GEO
Project description:NFAT1 is a transcription factor that elicits breast carcinoma cells to become invasive, contributing thus to formation of metastases. The molecular mechanisms by which NFAT1 operates in this respect are still poorly known. Here, we report that NFAT1 increases Lipocalin 2 (LCN2) mRNA and protein expression by binding to specific sites in the LCN2 gene promoter region. We show that the LCN2 protein is required downstream of NFAT1 to increase breast cancer cell invasion. We demonstrate that the NFAT1/LCN2 axis is sufficient to regulate expression of the TNF-like receptor TWEAKR at the RNA level and of its ligand, TWEAK, at the protein level. We show, however, that TWEAKR mediates an anti-invasive effect in breast cancer cells whereas, depending on LCN2 expression, TWEAK has either anti- and pro-invasive capacities. Thus, we identify LCN2 and TWEAKR/TWEAK as critical downstream effectors of NFAT1 to regulate breast cancer cell motility and invasive capacity.
2015-05-31 | GSE38369 | GEO