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MicroRNAs expression in kidneys from normal, cisplatin induced AKI rats and those with the restoration of MSCs

ABSTRACT: The availability of mesenchymal stem cells in kidney injury repair has been demonstrated. However, the underlying molecular mechanism remains not well understood. Herein, we profiled the altered microRNAs in renal tissiues from cisplatin-induced acute kidney injury (AKI) rats administrated with or without rat bone marrow mesenchymal stem cells, normal kidneys as control. Sprague Dawley rats were administrated with PBS by caudal vein after 24h peritoneal injection of 6mg/mg cisplatin, short for g2. 1×106 MSCs were injected to rats after 24h peritoneal injection of cisplatin, short for g3. Kidneys from healthey rats were used as control, short for g1. Renal tissues were collected at day 5 after treatment. There were 44 micorRNAs changed with significance between g2 and g3, among which 36 microRNAs upregulated and 8 microRNAs downregulated.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE66761 | GEO | 2015/03/11

SECONDARY ACCESSION(S): PRJNA277873

REPOSITORIES: GEO

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Project description:Neuroblastoma (NB) is an aggressive tumor that affects both infants and children. The disease outcome is greatly influenced by age of patient, stage, chromosome copy number aberrations (CNAs) and gene expression abnormalities. We analyzed, by microarray technology, genome and transcriptome of 3 groups of tumors of patients with metastatic disease: G1, stage 4S and MYCN single copy; G2, stage 4 younger than 18 months of age, MYCN single copy with no disease progression and G3, stage 4, older than 19 months, with unfavorable outcome. We found an accumulation of structural copy number aberrations (CNAs) in G3 whereas G1 tumors had mostly numerical (N) CNAs and G2 showed an intermediate behavior. Pair wise comparisons demonstrated that the average of N CNAs significantly decreased from G1 to G2 to G3 (9.6 G1 < 7.2 G2 < 3.6 G3); in contrast S CNAs significantly increased in G3 (0.7 G1 < 3.7 G2 < 7.0 G3). Interestingly, we observed several intra-chromosomal rearrangements in G3 tumors on chromosomes not usually involved in NB. Excluding MYCN amplified tumors by G3 we found a high frequency of S CNAs in this group. Gene expression analysis showed a deregulation of downstream genes of Ras and Rho signaling pathway among the 3 groups. It has been also observed a progressive switch off of development and adhesion genes and a switch on of cell cycle genes from G1 to G2 to G3. Moreover, the telemorase genes were significantly expressed in G3 with respect to remaining groups. Present data show an accumulation of S CNAs from stage 4S to 4. The deregulation of genes Rho/Ras pathway may explain the increase of tumor aggressiveness from G1 to G2 to G3. The increase of cell cycle and telomerase genes expression associated with G3 would provide unlimited replicative potential for these tumors and may be responsible for accumulation of S CNAs. Finally, we can argue that accumulation of structural aberrations and gene deregulation is age-dependent and it is associated with a more aggressive tumor phenotype.

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MicroRNAs expression in kidneys from normal, cisplatin induced AKI rats and those with the restoration of MSCs

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