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Analysis of altered LncRNA expression profiles in proximal renal tubular cells in response to calcium oxalate monohydrate crystal adhesion

ABSTRACT: The present study aims to assess the potential changes in LncRNAs of proximal renal cells in response to the adhesion of calcium oxalate monohydrate (COM) crystals.

ORGANISM(S): Homo sapiens

PROVIDER: GSE57111 | GEO | 2014/04/26

SECONDARY ACCESSION(S): PRJNA245447

REPOSITORIES: GEO

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Analysis of altered microRNA expression profiles in proximal renal tubular cells in response to calcium oxalate monohydrate crystal adhesion

Project description:The present study aims to assess the potential changes in microRNAs of proximal renal tubular cells in response to the adhesion of calcium oxalate monohydrate (COM) crystals. microRNA microarray was applied to evaluate the expression of HK-2 cells exposed to COM crystals for 0 and 24 hours.

2014-04-22 | E-GEOD-56934 | biostudies-arrayexpress

Analysis of altered LncRNA expression profiles in proximal renal tubular cells in response to calcium oxalate monohydrate crystal adhesion

Project description:The present study aims to assess the potential changes in LncRNAs of proximal renal cells in response to the adhesion of calcium oxalate monohydrate (COM) crystals. lncRNA microarray were applied to evaluate the expression of HK-2 cells exposed to COM crystal for 0 and 24 hours.

2014-04-26 | E-GEOD-57111 | biostudies-arrayexpress

Analysis of altered microRNA expression profiles in proximal renal tubular cells in response to calcium oxalate monohydrate crystal adhesion

Project description:The present study aims to assess the potential changes in microRNAs of proximal renal tubular cells in response to the adhesion of calcium oxalate monohydrate (COM) crystals.

2014-04-22 | GSE56934 | GEO

Effects of secretome derived from macrophages exposed to calcium oxalate crystals on renal fibroblast activation

Project description:The association between kidney stone disease and renal fibrosis has been widely explored in recent years but its underlying mechanisms remain far from complete understanding. Using label-free quantitative proteomics (nanoLC-ESI-LTQ-Orbitrap MS/MS), this study identified 23 significantly altered secreted proteins from calcium oxalate monohydrate (COM)-exposed macrophages (COM-MP) compared with control macrophages (Ctrl-MP) secretome. Functional annotation and protein-protein interactions network analysis revealed that these altered secreted proteins were involved mainly in inflammatory response and fibroblast activation. BHK-21 renal fibroblasts treated with COM-MP secretome had more spindle-shaped morphology with greater spindle index. Immunofluorescence study and gelatin zymography revealed increased levels of fibroblast activation markers (α-smooth muscle actin and F-actin) and fibrotic factors (fibronectin and matrix metalloproteinase-9 and -2) in the COM-MP secretome-treated fibroblasts. Our findings indicate that proteins secreted from macrophages exposed to COM crystals induce renal fibroblast activation and may play important roles in renal fibrogenesis in kidney stone disease.

2021-11-03 | PXD027039 | Pride

Expression factors for oxalate stimulation in HEK293T cells

Project description:parental HEK293T were challenged with 1064 µg/cm2 calcium oxalate monohydrate (COM) or sodium oxalate (NaOx) 4mM or vehicle for 24 hours and DNA microarray was performed. We observed and selected two-fold upregulation of laminin, beta 3 (LAMB3), early growth response 1 (EGR1), gremlin 1, DAN family BMP antagonist, Ca++-dependent secretion activator 2, Ras association domain family member 3, interleukin 33 and bone morphogenetic protein 8a , and two-fold down-regulation of interleukin 37 and intercellular adhesion molecule 1 in COM lord compared to vhicle.

2021-10-29 | GSE186676 | GEO

Analysis of microRNA expression profiles in exosomes of proximal renal tubular cells in response to oxalate crystal

Project description:The present study aims to compare the miRNA expression profiles in exosomes derived from HK-2 cells treated with 0, 1, 2 mM sodium oxalate, and to explore the roles of different exosomal-miRNAs in the regulation of calcium oxalate (CaOx) stones formation.

2018-02-13 | GSE110509 | GEO

EZH2-mediated macrophage-to-myofibroblast transition contributes to calcium oxalate crystal-induced kidney fibrosis

Project description:Long-term nephrocalcinosis leads to kidney injury, fibrosis, and even chronic kidney disease (CKD). Reports have proved macrophages can transition into myofibroblasts(MMT), leading to collagen deposition and fibrosis in CKD. However, the effect of MMT in calcium oxalate (CaOx) crystal-induced kidney fibrosis remains unclear. This study demonstrated that histone methyltransferase EZH2-mediated MMT contributes to CaOx crystal-induced fibrosis. We identified abundant MMT cells by immunofluorescence and flow cytometry in kidney tissues of patients with CaOx-related CKD, CaOx nephrocalcinosis mouse model, and CaOx-treated RAW264.7 macrophage cells. A high level of MMT cell infiltration was associated with a decline in the glomerular filtration rate in CaOx nephrocalcinosis patients. Clodronate Liposomes-mediated macrophage depletion attenuates calcium oxalate crystal-induced fibrosis in mice. Subsequently, transcriptomic and single-cell sequencing revealed that EZH2 was highly expressed in kidneys with CaOx deposition, especially in macrophages. Further study demonstrated that EZH2 inducible knock-out or pharmacological inhibition by GSK-126 attenuated MMT and renal fibrosis in vivo and in vitro. Mechanistically, ChIP and transcriptomic sequencing showed that EZH2 inhibition reduced the enrichment of H3K27me3 on the DUSP23 gene promoter and elevated DUSP23 expression. The Co-IP and molecular docking analysis showed that DUSP23 mediated the dephosphorylation of pSMAD3 (S423/425), the key regulator of MMT. In addition, DUSP23 over-expression could alleviate SMAD3-mediated MMT. Thus, our study found that EZH2 promotes kidney fibrosis by meditating MMT via the DUSP23/SMAD3 pathway in nephrocalcinosis.

2024-10-26 | GSE280007 | GEO

Analysis of altered microRNA expression profiles in proximal renal tubular cells in response to calcium oxalate monohydrate crystal adhesion: implications for kidney stone disease.

Project description:BackgroundCalcium oxalate monohydrate (COM) is the major crystalline component in kidney stones and its adhesion to renal tubular cells leads to tubular injury. However, COM-induced toxic effects in renal tubular cells remain ambiguous. MicroRNAs (miRNAs) play an important role in gene regulation at the posttranscriptional levels.ObjectiveThe present study aimed to assess the potential changes in microRNAs of proximal renal tubular cells in response to the adhesion of calcium oxalate monohydrate (COM) crystals.MethodologyLactate dehydrogenase (LDH) activity and DAPI staining were used to measure the toxic effects of HK-2 cells exposed to COM crystals. MicroRNA microarray and mRNA microarray were applied to evaluate the expression of HK-2 cells exposed to COM crystals. Quantitative real-time PCR (qRT-PCR) technology was used to validate the microarray results. Target prediction, Gene Ontology (GO) analysis and pathway analysis were applied to predict the potential roles of microRNAs in biological processes.Principal findingsOur study showed that COM crystals significantly altered the global expression profile of miRNAs in vitro. After 24 h treatment with a dose (1 mmol/L), 25 miRNAs were differentially expressed with a more than 1.5-fold change, of these miRNAs, 16 were up-regulated and 9 were down-regulated. A majority of these differentially expressed miRNAs were associated with cell death, mitochondrion and metabolic process. Target prediction and GO analysis suggested that these differentially expressed miRNAs potentially targeted many genes which were related to apoptosis, regulation of metabolic process, intracellular signaling cascade, insulin signaling pathway and type 2 diabetes.ConclusionOur study provides new insights into the role of miRNAs in the pathogenesis associated with nephrolithiasis.

| S-EPMC4077747 | biostudies-literature

Calcium oxalate crystal induced transcriptomic changes in renal epithelial cells.

Project description:Small molecule inhibiton of calcium oxalate induced transcriptomic changes of renal epithelial cells.

| PRJEB34728 | ENA

Calcium oxalate crystals and oxalate induce an epithelial-to-mesenchymal transition in the proximal tubular epithelial cells: Contribution to oxalate kidney injury.

Project description:TGF-β1 is the main mediator of epithelial-to-mesenchymal transition (EMT). Hyperoxaluria induces crystalluria, interstitial fibrosis, and progressive renal failure. This study analyzed whether hyperoxaluria is associated with TGF-β1 production and kidney fibrosis in mice and if oxalate or calcium oxalate (CaOx) could induce EMT in proximal tubule cells (HK2) and therefore contribute to the fibrotic process. Hyperoxaluria was induced by adding hydroxyproline and ethylene glycol to the mice's drinking water for up to 60 days. Renal function and oxalate and urinary crystals were evaluated. Kidney collagen production and TGF-β1 expression were assessed. EMT was analyzed in vitro according to TGF-β1 production, phenotypic characterization, invasion, cell migration, gene and protein expression of epithelial and mesenchymal markers. Hyperoxaluric mice showed a decrease in renal function and an increase in CaOx crystals and Ox urinary excretion. The deposition of collagen in the renal interstitium was observed. HK2 cells stimulated with Ox and CaOx exhibited a decreased expression of epithelial as well as increased expression mesenchymal markers; these cells presented mesenchymal phenotypic changes, migration, invasiveness capability and TGF-β1 production, characterizing EMT. Treatment with BMP-7 or its overexpression in HK2 cells was effective at preventing it. This mechanism may contribute to the fibrosis observed in hyperoxaluria.

| S-EPMC5384284 | biostudies-literature

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