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ABSTRACT: Inhibition of NLRP3 alleviates calcium oxalate crystal-induced renal fibrosis and crystal adhesion

PROVIDER: PRJNA1203736 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31842515_1.fastq.gz	Fastqsanger.gz
	SRR31842515_2.fastq.gz	Fastqsanger.gz
	SRR31842516_1.fastq.gz	Fastqsanger.gz
	SRR31842516_2.fastq.gz	Fastqsanger.gz
	SRR31842517_1.fastq.gz	Fastqsanger.gz

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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

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 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.

2014-04-26 | GSE57111 | GEO

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

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

Calcium oxalate crystals with a bipyramidal morphology and a high tendency to aggregate attach directly to breast cancer cells and affect their phenotype

Project description:Various types of crystal can form in our bodies under normal and pathological conditions, with the more harmful of these crystals being studied intensively. However, much less is known about calcium oxalate dihydrate (COD) crystals, which are commonly associated with benign conditions. In general, calcium oxalates are pathological biominerals found in kidney stones and as microcalcifications (MCs) in breast and thyroid cancers. In breast cancer MCs, COD crystals are exclusively associated with benign lesions, and we have recently shown that they suppress breast precancer progression in vitro. Here, we studied the influence of synthetic calcium oxalate crystals – both COD and calcium oxalate monohydrate (COM) – with different morphologies and properties on crystal-cell interactions. We found that the less negatively charged crystals exhibited a greater tendency to aggregate and, as aggregates, attached better to cells, particularly to the cells of an invasive breast cancer cell line. We did not find any association between crystallinity, surface area, and solubilities of the crystals and attachment to cells. The crystal types that did attach efficiently to the cells, namely, COD with a thin or thick bipyramidal morphology, had the greatest impact on cell phenotype and functionally delayed cell growth, most probably through contact inhibition. Notably, in terms of morphology and size, these crystals resembled COD MCs found in benign breast tissues, suggesting that they are involved in a mechanism of tumor suppression.

2026-07-29 | GSE308114 | GEO

Genome-wide analysis of renal gene expression during hyperoxaluria development

Project description:Previous studies have proposed that production of reactive oxygen species (ROS) is an important contributor to renal injury and inflammation following exposure to oxalate or calcium-oxalate crystals. The present study was conducted to determine, utilizing global transcriptome analyses, if the NADPH oxidase system is activated in kidneys of rats fed a diet leading to hyperoxaluria and crystal deposition. HLP was used to induce hyperoxaluria. Hyperoxaluria will lead to crystallization and up regulation of various NADPH oxidase subunits followed by increased expression of different specific genes. It is our hypothesis that crystallization induces inflammation of the kidneys via the activation of renin-angiotensin system (RAS) and production of reactive oxygen species (ROS) through NADPH oxidase complex. Apocynin was used to block hyperoxaluria and production of reactive oxygen species (ROS) with the inhibition of NADPH oxidase system as Apocynin inhibits membrane translocation of p47 subunit of NADPH oxidase.

2012-12-20 | GSE36446 | GEO

Homo sapiens

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

| PRJNA245447 | ENA

Homo sapiens

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

| PRJNA245009 | ENA

C-reactive protein promotes diabetic kidney disease via Smad3 mediated NLRP3 inflammasome activation

Project description:Diabetic kidney disease (DKD) is the leading cause of end-stage kidney diseases resulting enormous social-economic burden. Accumulated evidence has indicated that C-reactive protein (CRP) exacerbates DKD by enhancing renal inflammation and fibrosis through TGF-β/Smad3 signaling. NLRP3 inflammasome is the key sensor contributing to renal inflammation. However, whether CRP enhances inflammation in DKD via NLRP3 inflammasome related pathway remains unknown. In this study, we demonstrate that CRP promotes DKD via Smad3-mediated NLRP3 inflammasome activation as mice overexpressing human CRP gene exhibits accelerated renal inflammation in diabetic kidneys, which is associated with the activation of Smad3 and NLRP3 inflammasome. In contrast, blockade of CPR signaling with a neutralizing anti-CD32 antibody attenuates CRP-induced activation of Smad3 and NLRP3 in vitro. Importantly, genetic deletion or pharmacological inhibition of Smad3 also mitigates CRP-induced activation of NLRP3 in diabetic kidneys or in high glucose treated cells. Mechanistically, we reveal that Smad3 binds to the NLRP3 gene promoter which is enhanced by CRP. Taken together, we conclude that CRP induces renal inflammation in DKD via to the Smad3-NLRP3 inflammasome-dependent mechanism. Thus, targeting CRP or Smad3-NLRP3 pathways may be a new therapeutic potential for DKD.

2025-01-29 | GSE271870 | GEO

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