Cloning and transplantation of adult renal tubular progenitors
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ABSTRACT:
PROVIDER: PRJNA491500 | ENA |
REPOSITORIES: ENA
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Project description:Cloning and variation of adult renal tubular progenitors
| PRJNA489235 | ENA
Project description:Kidney damage involves the progressive and inexorable destruction of tubular and glomerular system. However, it is known that the patients survive AKI often recover renal structure and function. Correspondingly, previous studies demonstrated tubular regeneration in mice after massive kidney injury and linked mouse Sox9+ renal progenitor cells to this process. Here we show that progenitor cells can be cloned from mouse medulla and cortex. Clones can be grown from a single cell and indefinitely passaged. Progenitor cells derived from renal medulla can readily assembly into “kidney organoids” expressing proximal/distal tubular cell markers in 3D culture.
2022-04-22 | GSE120049 | GEO
Project description:Kidney damage involves the progressive and inexorable destruction of tubular and glomerular system. However, it is known that the patients survive AKI often recover renal structure and function. Correspondingly, previous studies demonstrated tubular regeneration in mice after massive kidney injury and linked mouse Sox9+ renal progenitor cells to this process. Here we show that renal progenitor cells can be cloned from renal needle biopsy sample of CKD patients. Progenitor cells can readily assembly into “kidney organoids” expressing proximal/distal tubular cell markers in 3D culture.
2022-04-22 | GSE119426 | GEO
Project description:Histological analysis of biopsy is the gold standard to assess renal allograft status. Furthermore, 1-year protocol biopsy is often performed to evaluated graft outcome. However, since biopsy cannot be performed in a time serial basis, we decided to investigate whether blood can be a good compartment to predict allograft outcome. Gene expression microarrays and a large phenotype have been performed in peripheral blood mononuclear cells from 79 renal transplanted patients taken 3 months after transplantation. We evaluated the association of biological parameters with 4 histological groups defined on renal biopsy taken at 1-year post-transplantation: patients which display normal biopsy (n=45), patients with signs of tubular atrophy and interstitial fibrosis (IFTA) (n=14), with IFTA with inflammation (i-IFTA) (n=14) and patients with alloimmune lesions (n=6) Transcriptomic profile using PBMC from patients showing normal biopsy (n=45), patients with signs of tubular atrophy and interstitial fibrosis (IFTA) (n=14), with IFTA with inflammation (i-IFTA) (n=14) and patients with alloimmune lesions (n=6).
2015-12-24 | E-GEOD-57731 | biostudies-arrayexpress
Project description:Epigenetic mechanisms as DNA methylation can affect allograft outcome after kidney transplantation, accelerating renal aging. Complement system is the major player of ischemia reperfusion (I/R) injury and Renal Proximal Tubular Cells (RPTEC) are known to express C5a receptor (C5aR). However, little is known about the downstream effect of C5a-C5aR interaction. We performed a whole-genome DNA methylation analysis on C5a stimulated RPTEC and found several regions regulating genes involved in cell cycle control, DNA damage checkpoints and WNT signaling. These most represented genes were BCL9, CYP1B1 and CDK6. We showed that C5a induced-aberrant gene methylation significantly influences the expression of these genes. Moreover, the stimulation of RTEC by C5a led to senescence by up-regulating SA-β Gal positivity and increasing p53 gene and p21 protein level. IL-6, MCP-1, CTGF gene levels increase indicated the tubular SASP (Senescence associated Secretory Phenotype) acquirement. In accordance, in a swine model of I/R injury, we found that the increase expression of WNT4/βcatenin expression correlated with the augment in SA-β Gal, p21, p16 and IL-6 positivity after 24h from reperfusion. The treatment with C1-INH, a complement inhibitor, efficiently antagonized SASP restoring SA-β Gal, p21, p16, IL-6 expression at basal level and abrogating the WNT4/βcatenin activation. Thus, C5a affects the DNA methylation of genes involved in tubular senescence leading to a persistent, low-grade, inflammatory state called inflammaging. Targeting epigenetic programs may offer novels strategies to protect tubular cells from aging and promote kidney repair and recovery.
2019-08-20 | GSE115227 | GEO
Project description:Histological analysis of biopsy is the gold standard to assess renal allograft status. Furthermore, 1-year protocol biopsy is often performed to evaluated graft outcome. However, since biopsy cannot be performed in a time serial basis, we decided to investigate whether blood can be a good compartment to predict allograft outcome. Gene expression microarrays and a large phenotype have been performed in peripheral blood mononuclear cells from 79 renal transplanted patients taken 3 months after transplantation. We evaluated the association of biological parameters with 4 histological groups defined on renal biopsy taken at 1-year post-transplantation: patients which display normal biopsy (n=45), patients with signs of tubular atrophy and interstitial fibrosis (IFTA) (n=14), with IFTA with inflammation (i-IFTA) (n=14) and patients with alloimmune lesions (n=6)
2015-12-24 | GSE57731 | GEO
Project description:The mechanistic target of rapamycin mTORC1 is a key regulator of cell metabolism and autophagy. Despite widespread clinical use of mTOR inhibitors, the role of mTORC1 in renal tubular function and kidney homeostasis remains elusive. By utilizing constitutive and inducible deletion of conditional Raptor alleles in renal tubular epithelial cells, we discovered that mTORC1 deficiency caused a marked concentrating defect, loss of tubular cells and slowly progressive renal fibrosis. Transcriptional profiling revealed that mTORC1 maintains renal tubular homeostasis by controlling mitochondrial metabolism and biogenesis as well as transcellular transport processes involved in counter-current multiplication and urine concentration. Although mTORC2 partially compensated the loss of mTORC1, exposure to ischemia and reperfusion injury exaggerated the tubular damage in mTORC1-deficient mice, and caused pronounced apoptosis, diminished proliferation rates and delayed recovery. These findings identify mTORC1 as an essential regulator of tubular energy metabolism and as a crucial component of ischemic stress responses. Pharmacological inhibition of mTORC1 likely affects tubular homeostasis, and may be particularly deleterious if the kidney is exposed to acute injury. Furthermore, the combined inhibition of mTORC1 and mTORC2 may increase the susceptibility to renal damage. Raptor fl/fl*KspCre and Raptor fl/fl animals were sacrificed at P14 before the development of an overt functional phenotype. Kidneys were split in half and immediately snap frozen in liquid nitrogen.
2014-06-09 | E-GEOD-54417 | biostudies-arrayexpress
Project description:Activation of hypoxia-inducible transcription factors (HIF) leading to expression of hundred of target genes is a fundamental mechanism in acute and chronic kidney disease mediating protective but also possibly harmful effects. Furthermore, dysregulation of the HIF pathway in chronic kidney disease causes renal anemia through insufficient induction of erythropoietin (EPO) in interstitial cells. Hence, pharmacological compounds to treat renal anemia by stabilizing HIF have recently been introduced to the clinical practice. RNA-seq analysis was performed in primary renal tubular cells to analyse the effect of HIF stabilization on the expression of pathogenic Mucin1 (MUC1) variants. This study links the regulation of the kidney-disease gene MUC1 with the HIF-pathway in renal tubular cells.
2023-06-07 | GSE224177 | GEO
Project description:To find miRNAs that involve in renal epithelial-mesenchyal transition induced by TGFbeta Mouse renal tubular cell, MCT (derived from SJL H-2S mice) was stimulated by TGFbeta 3ng/ml for 72 hours. miRNA expressions were compared with control.
2012-12-05 | E-GEOD-42718 | biostudies-arrayexpress
Project description:Shiga toxin type 2 (Stx2) from Escherichia coli is thought to be a main factor to casue renal dysfunction in Enterohemorrhagic E. coli (EHEC) infection. The renal dysfunction caused by the proximal tubular defects can be detected in the earlier EHEC infection. However, the precise information of gene expression from proximal tubular epithelial cells has yet to be clarified. We performed microarray experiments using Stx2-injected mouse kidney and Stx2-treated human renal proximal tubular epithelial cells (RPTEC), and extracted common genes that were differentially expressed.
2022-01-01 | GSE172466 | GEO