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Gene expression profiles in isolated proximal tubules and whole kidneys of rats after cisplatin-administration

ABSTRACT: To clarify the effects of cisplatin (cis-diamminedichloroplatinum II, CDDP) on the gene expression profiles in renal proximal tubules, microarray analyses were carried out using total RNA samples isolated from microdissected proximal tubules and whole kidneys. The molecular events underlying acute kidney injury (AKI) in the proximal tubules of rats with cisplatin-induced nephrotoxicity were successfully clarified with 17,000 transcripts. Renal proximal tubules were isolated under microscopy, and transcriptome data were collected with Rat Genome Survey MicroarrayÂ® (Applied Biosystems)

ORGANISM(S): Rattus norvegicus

SUBMITTER: Satohiro Masuda

PROVIDER: E-GEOD-37133 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression profiles in isolated proximal tubules and whole kidneys of rats after cisplatin-administration

Project description:To clarify the effects of cisplatin (cis-diamminedichloroplatinum II, CDDP) on the gene expression profiles in renal proximal tubules, microarray analyses were carried out using total RNA samples isolated from microdissected proximal tubules and whole kidneys. The molecular events underlying acute kidney injury (AKI) in the proximal tubules of rats with cisplatin-induced nephrotoxicity were successfully clarified with 17,000 transcripts.

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Transcription profiling of human kidney glomerular and tubular progenitor cells

Project description:Multipotent progenitor cells (MPs) have been observed in human kidneys and particularly in Bowman's capsule and proximal tubules. The kidney owns the ability to repair local damage and renal MPs may play a role in the regenerative processes. Microarray technology was applied to identify differentially expressed genes among resident MPs isolated from glomeruli and tubules of normal renal tissue, renal proximal tubular epithelial cells (RPTECs) and mesenchymal stem cells (MSCs). The results of our analysis represent a starting point for further functional studies. Experiment Overall Design: This study includes three renal tissue samples which were processed to obtain 3 glomerular progenitor populations and 3 tubular ones. Three subcoltures of MSCs and RPTECs were included as well. The differences in gene expression patterns of the 4 cell types were found out.

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Project description:In this study, we profiled the change of gene expression by p53 knock-down on anaplastic thyroid carcinoma (ATC) cell line, KAT-18 cells using Applied Biosystem's Microarrays. When compared with the untreated control KAT-18 cells, 2,926 genes were found to have altered expression levels of 2-fold or more in cells treated with antisense p53 oligonucleotide. Microarray analysis revealed that p53 knock-down modified the expression of numerous apoptosis-related genes. Among those genes, 33 apoptosis pathway activators and 20 apoptosis pathway repressors were identified. We analyzed human thyroid carcinoma cell (KAT18) on Applied Biosystem Human 1700 Chip Arrays. There were control and test sample, respectively, KAT18 untreated and treated antisense p53.

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The soluble intracellular domain of megalin does not affect renal proximal tubular function in vivo

Project description:The endocytic receptor megalin constitutes the main pathway for clearance of plasma proteins from the glomerular filtrate in the proximal tubules. However, little is know about the mechanisms that control receptor activity. A widely discussed hypothesis states that the intracellular domain (ICD) of megalin, released upon ligand binding, acts as a transcription regulator to suppress receptor expression - a mechanism proposed to safeguard the proximal tubules from protein overload. Here, we have put this hypothesis to the test by generating a mouse model co-expressing the soluble ICD and the full-length receptor. Despite pronounced expression in the proximal tubules, the ICD failed to exert any effects on renal proximal tubular function such as megalin expression, protein retrieval, or renal gene transcription. Thus, our data argue that the ICD does not play a role in regulation of megalin activity in vivo in the proximal tubules. We used microarrays to compare gene expression profile in adult kidney from a new mouse model expressing the intracellular domain of megalin with wildtype. 10 week old mice were collected for RNA extraction and hybridization on Affymetrix microarrays. Three individuals for each genotype were analyzed comparing heterozygous animals for the intracellular domain of megalin with littermates controls.

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2013-12-31 | E-GEOD-50507 | biostudies-arrayexpress

The soluble intracellular domain of megalin does not affect renal proximal tubular function in vivo

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Inhibition of prolyl hydroxylase promotes the reprogramming of Sox9+ renal progenitor cells and renal regeneration

Project description:Mammalian kidney has very limited ability to repair or regenerate after acute kidney injury (AKI). The maladaptive repair of AKI promotes the progression to chronic kidney disease (CKD). Therefore, it is extremely urgent to explore new strategies to promote the repair/regeneration of injured renal tubules after AKI. It has been shown that hypoxia induces heart regeneration in adult mice. However, it is unknown whether hypoxia can induce kidney regeneration after AKI. In this study, we used a prolyl hydroxylase domain inhibitor (PHDI), MK-8617, to mimic hypoxia condition and found that MK-8617 significantly ameliorates ischemia reperfusion injury (IRI) induced acute kidney injury. We then showed that MK-8617 dramatically facilitates renal regeneration via promoting the proliferation of injured renal proximal tubular cells (RPTCs) after IRI-induced AKI. We then performed bulk mRNA sequencing and discovered that multiple nephrogenesis- related genes were significantly upregulated with MK-8617 pretreatment. Furthermore, we showed that MK-8617 may alleviate proximal tubule injury via stabilizing HIF-1α protein specifically in renal proximal tubular cells. We also demonstrated that MK-8617 promotes the reprogramming of renal proximal tubular cells to Sox9+ renal progenitor cells, and the regeneration of renal proximal tubules. In summary, we discovered that inhibition of prolyl hydroxylase improves renal proximal tubule regeneration after IRI-induced AKI via promoting the reprogramming of renal proximal tubular cells to Sox9+ renal progenitor cells.

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