Ontology highlight
ABSTRACT:
PROVIDER: PRJNA783810 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17043500_1.fastq.gz | Fastqsanger.gz | |||
| SRR17043500_2.fastq.gz | Fastqsanger.gz | |||
| SRR17043501_1.fastq.gz | Fastqsanger.gz | |||
| SRR17043501_2.fastq.gz | Fastqsanger.gz | |||
| SRR17043502_1.fastq.gz | Fastqsanger.gz |
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Project description:In numerous forms of organ injury, interstitial fibrosis is a final common pathway. Despite recent epidemiological studies, therapies to focus on fibrosis and to delay progressive renal failure are limited. Previously our group showed that sphingosine kinase 2 deficient-mice (SphK2-/-) develop less fibrosis in folic acid-induced or unilateral ischemia-reperfusion injury (IRI)-induced kidney fibrosis models. Sphingosine 1-phosphate (S1P) is produced by two sphingosine kinase isoforms (SphK1 and SphK2). S1P is involved in diverse functions, but the role of S1P produced by SphK2 is gathering attention as treatments focused on epigenetics have been developed. SphK2 is primarily located in the nucleus and S1P produced by SphK2 inhibits histone deacetylase (HDAC) and changes in histone acetylation status, which can lead to an altered target gene expression. We identified that bone marrow stromal cell antigen-1 (Bst1/CD157) is a gene related with kidney fibrosis based on the combination of genome-wide analysis and in vivo screening. SphK2 regulates Bst1 expression and Bst1-/- mice develop less fibrosis after unilateral IRI and are protected against renal bilateral IRI. Bone marrow chimera experiments further revealed the importance of Bst1 expression on hematopoietic cells. Furthermore we identified the role of Bst1 expression in neutrophils for inducing renal ischemia-reperfusion injury and fibrosis.
2019-09-01 | GSE103058 | GEO
Project description:Chronic kidney disease (CKD) is a burden for Public Health and concerns millions of individuals worldwide. Independently of the cause, CKD is secondary to the replacement of functional renal tissue by extra-cellular matrix proteins (i.e fibrosis) that progressively impairs kidney function. The pathophysiological pathways that control the development of renal fibrosis are common to most of the nephropathies involving native kidneys or kidney grafts. Unfortunately, very few treatments are available to stop renal fibrosis and most of the therapeutic strategies are often barely able to slow down the progression of fibrogenesis in native kidneys. Therefore, it is mandatory to discover new therapeutic pathways to stop renal fibrosis. Our objective is to study new pathways involved in renal fibrosis. We thus decided to use the model of Unilateral Ureteral renal Obstruction in mice, a fast and reproducible experimental model of renal fibrosis. We studied renal fibrosis using experimental model of ureteral unilateral obstruction in mice, which was performed by complete ligation of the left ureter. The control lateral right kidney served as internal control.
2013-02-10 | E-GEOD-38117 | biostudies-arrayexpress
Project description:Renal fibrosis is the final common pathway for chronic kidney disease. However, the detailed mechanisms and therapeutic strategies for renal fibrosis have not been established. MicroRNAs (miRNAs) are small, non coding RNAs that regulate various pathological conditions and diseases. Previous studies reported that miRNAs play a pivotal role in renal fibrosis. However, the role of miRNAs in renal fibrosis has not been completely elucidated. Therefore, in this study, miRNAs on renal fibrosis was investigated in a renal fibrosis mouse model generated by unilateral ureteral obstruction. MiRNA microarray analysis revealed 109 miRNAs that were upregulated more than 2 fold and 113 miRNAs that were downregulated less than 0.5 fold in the kidney of UUO mice compared with control mice.
2021-01-07 | GSE162794 | GEO
Project description:In numerous forms of organ injury, interstitial fibrosis is a final common pathway. Despite recent epidemiological studies, therapies to focus on fibrosis and to delay progressive renal failure are limited. Previously our group showed that sphingosine kinase 2 deficient-mice (SphK2-/-) develop less fibrosis in folic acid-induced or unilateral ischemia-reperfusion injury (IRI)-induced kidney fibrosis models. Sphingosine 1-phosphate (S1P) is produced by two sphingosine kinase isoforms (SphK1 and SphK2). S1P is involved in diverse functions, but the role of S1P produced by SphK2 is gathering attention as treatments focused on epigenetics have been developed. SphK2 is primarily located in the nucleus and S1P produced by SphK2 inhibits histone deacetylase (HDAC) and changes in histone acetylation status, which can lead to an altered target gene expression. We identified that bone marrow stromal cell antigen-1 (Bst1/CD157) is a gene related with kidney fibrosis based on the combination of genome-wide analysis and in vivo screening. SphK2 regulates Bst1 expression and Bst1-/- mice develop less fibrosis after unilateral IRI and are protected against renal bilateral IRI. Bone marrow chimera experiments further revealed the importance of Bst1 expression on hematopoietic cells. Furthermore we identified the role of Bst1 expression in neutrophils for inducing renal ischemia-reperfusion injury and fibrosis.
2019-09-01 | GSE103062 | GEO
Project description:Neuropilin-1 (NRP1), a co-receptor for various cytokines, including TGF-β, has been identified as a potential therapeutic target for fibrosis. However, its role and mechanism in renal fibrosis remains elusive. Here, we show that NRP1 is upregulated in distal tubular (DT) cells of patients with transplant renal insufficiency and mice with renal ischemia-reperfusion (I-R) injury. Knockout of Nrp1 reduced multiple endpoints of renal injury and fibrosis. We found that Nrp1 facilitates the binding of TNF-α to its receptor in DT cells after renal injury. This signaling results in a downregulation of lysine crotonylation of the metabolic enzyme Cox4i1, decreased cellular energetics and exacerbation of renal injury. Furthermore, by single-cell RNA-sequencing we found that Nrp1-positive DT cells secrete collagen and communicate with myofibroblasts, exacerbating acute kidney injury (AKI)-induced renal fibrosis by activating Smad3. Dual genetic deletion of Nrp1 and Tgfbr1 in DT cells better improves renal injury and fibrosis than either single knockout. Together, these results reveal that targeting of NRP1 represents a promising strategy for the treatment of AKI and subsequent chronic kidney disease.
2024-06-03 | PXD052293 | Pride
Project description:Neuropilin-1 (NRP1), a co-receptor for various cytokines, including TGF-β, has been identified as a potential therapeutic target for fibrosis. However, its role and mechanism in renal fibrosis remains elusive. Here, we show that NRP1 is upregulated in distal tubular (DT) cells of patients with transplant renal insufficiency and mice with renal ischemia-reperfusion (I-R) injury. Knockout of Nrp1 reduced multiple endpoints of renal injury and fibrosis. We found that Nrp1 facilitates the binding of TNF-α to its receptor in DT cells after renal injury. This signaling results in a downregulation of lysine crotonylation of the metabolic enzyme Cox4i1, decreased cellular energetics and exacerbation of renal injury. Furthermore, by single-cell RNA-sequencing we found that Nrp1-positive DT cells secrete collagen and communicate with myofibroblasts, exacerbating acute kidney injury (AKI)-induced renal fibrosis by activating Smad3. Dual genetic deletion of Nrp1 and Tgfbr1 in DT cells better improves renal injury and fibrosis than either single knockout. Together, these results reveal that targeting of NRP1 represents a promising strategy for the treatment of AKI and subsequent chronic kidney disease
2024-06-03 | PXD052244 | Pride
Project description:Renal fibrosis is present in all forms of chronic kidney disease (CKD) and when dysregulated contributes to renal failure. Renal fibroblast is the major precursor to myofibroblast, the effector cell type of renal fibrosis. In the present study we investigated the role of Suv39h1, a lysine methyltransferase, in fibroblast-myofibroblast transition (FMyT) and renal fibrosis. We report that Su39h1 is up-regulated during FMyT both in vitro and in vivo. Suv39h1 deletion in fibroblasts partially blocked FMyT in vitro and attenuated renal fibrosis in three different animal models. Additionally, conditional Suv39h1 knockout in Postn+ mature myofibroblasts mitigated renal fibrosis in mice. Importantly, Suv39h1 inhibition with a small-molecule compound chaetocin suppressed FMyT in cell culture and ameliorated renal fibrosis in mice. Transcriptomic analysis uncovered CXCL10 as a downstream target for Suv39h1. CXCL10 knockdown nullified the protective effect of Suv39h1 insufficiency on renal fibrosis. Mechanistically, CXCL10 regulated FMyT by suppressing the Hippo/YAP pathway. In conclusion, our data illustrate a previously unrecognized role for Suv39h1 in regulating renal fibrosis.
2025-10-01 | GSE246192 | GEO
Project description:Renal fibrosis is present in all forms of chronic kidney disease (CKD) and when dysregulated contributes to renal failure. Renal fibroblast is the major precursor to myofibroblast, the effector cell type of renal fibrosis. In the present study we investigated the role of Suv39h1, a lysine methyltransferase, in fibroblast-myofibroblast transition (FMyT) and renal fibrosis. We report that Su39h1 is up-regulated during FMyT both in vitro and in vivo. Suv39h1 deletion in fibroblasts partially blocked FMyT in vitro and attenuated renal fibrosis in three different animal models. Additionally, conditional Suv39h1 knockout in Postn+ mature myofibroblasts mitigated renal fibrosis in mice. Importantly, Suv39h1 inhibition with a small-molecule compound chaetocin suppressed FMyT in cell culture and ameliorated renal fibrosis in mice. Transcriptomic analysis uncovered CXCL10 as a downstream target for Suv39h1. CXCL10 knockdown nullified the protective effect of Suv39h1 insufficiency on renal fibrosis. Mechanistically, CXCL10 regulated FMyT by suppressing the Hippo/YAP pathway. In conclusion, our data illustrate a previously unrecognized role for Suv39h1 in regulating renal fibrosis.
2025-10-01 | GSE246190 | GEO
Project description:Renal fibrosis is present in all forms of chronic kidney disease (CKD) and when dysregulated contributes to renal failure. Renal fibroblast is the major precursor to myofibroblast, the effector cell type of renal fibrosis. In the present study we investigated the role of Suv39h1, a lysine methyltransferase, in fibroblast-myofibroblast transition (FMyT) and renal fibrosis. We report that Su39h1 is up-regulated during FMyT both in vitro and in vivo. Suv39h1 deletion in fibroblasts partially blocked FMyT in vitro and attenuated renal fibrosis in three different animal models. Additionally, conditional Suv39h1 knockout in Postn+ mature myofibroblasts mitigated renal fibrosis in mice. Importantly, Suv39h1 inhibition with a small-molecule compound chaetocin suppressed FMyT in cell culture and ameliorated renal fibrosis in mice. Transcriptomic analysis uncovered CXCL10 as a downstream target for Suv39h1. CXCL10 knockdown nullified the protective effect of Suv39h1 insufficiency on renal fibrosis. Mechanistically, CXCL10 regulated FMyT by suppressing the Hippo/YAP pathway. In conclusion, our data illustrate a previously unrecognized role for Suv39h1 in regulating renal fibrosis.
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