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Pkd2-dependent transcriptome profile in a newly estabilshed mouse Pkd2 knockout cell line

ABSTRACT: Purpose: The goal of this study is to explore early changes of gene expression in the new mouse kidney Pkd2 knockout cell model. To identify compreshensive expressional changes of genes by Pkd2 knockout, transcriptomic changes by Pkd2 knockout induced by doxycycline treatment for 6 days at two different passages were profiled and analyzed. Methods: Total RNAs were isolated from cells treated with or without doxycycline for 6 days. Four replicates of each group were generated. cDNA libraries were prepared and sequenced on Illumina HiSeq4000 platform and then sequence reads were qualified and quantified. Differential expression analysis were performed using edgeR. Results: mRNA profiles of the new mouse kidney Pkd2 knockout cell model treated with doxycycline for 6 days were generated using an optimized RNA-Seq workflow. Transcript level quantification using the STAR quant mode was performed to calculate transcript abundance in each sample. Then differential expression analysis identified the differentially expressed genes at different passages of cell culture. Conclusions: This study revealed early transcriptomic changes dependent on Pkd2 in a new in vitro Pkd2 knockout cell model of the mouse kidney.

ORGANISM(S): Mus musculus

PROVIDER: GSE171574 | GEO | 2023/09/13

REPOSITORIES: GEO

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Project description:Polycystic Kidney Disease is characterized by the formation of large fluid-filled cysts that eventually destroy the renal parenchyma leading to end-stage renal failure. Although remarkable progress has been made in understanding the pathologic mechanism of the disease, the precise orchestration of the early events leading to cyst formation is still unclear. Abnormal cellular proliferation was traditionally considered to be one of the primary irregularities leading to cyst initiation and growth. Consequently, many therapeutic interventions have focused on targeting this abnormal proliferation, and some have even progressed to clinical trials. However, the role of proliferation in cyst development was primarily examined at stages where cysts are already visible in the kidneys and therefore at later stages of disease development. In this study we focused on the cystic phenotype since birth in an attempt to clarify the temporal contribution of cellular proliferation in cyst development. Using a PKD2 transgenic rat model (PKD2 (1-703)) of different ages (0-60 days after birth) we performed gene expression profiling and phenotype analysis by measuring various kidney parameters. Phenotype analysis demonstrated that renal cysts appear immediately after birth in the PKD2 transgenic rat model (PKD2 (1-703)). On the other hand, abnormal proliferation occurs at later stages of the disease as identified by gene expression profiling. Interestingly, other pathways appear to be deregulated at early stages of the disease in this PKD model. Our data suggest that cystogenesis precedes deregulation of proliferation-related pathways, suggesting that proliferation abnormalities may contribute in cyst growth rather than cyst formation. In this study we focused on the cystic phenotype since birth in an attempt to clarify the temporal contribution of cellular proliferation in cyst development. Using a PKD2 transgenic rat model (PKD2 (1-703)) of different ages (0,6 and 24 days after birth) we performed gene expression profiling of kidney cells.

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Pkd2-dependent transcriptome profile in a newly estabilshed mouse Pkd2 knockout cell line

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