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Next Generation Sequencing of Pkd1 mutant kidneys

ABSTRACT: This study sough to understand the differential gene expression profile of Pkd1 mutant mice kidneys in the setting of miR 17~92 deletion

ORGANISM(S): Mus musculus

PROVIDER: GSE89764 | GEO | 2017/06/12

SECONDARY ACCESSION(S): PRJNA353115

REPOSITORIES: GEO

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Gene expression profiling of kidneys derived from Pkd1 conditional knock-out (KO) mice treated by Salsalate

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Next Generation Sequencing of PKD2 mutant mice kidneys

Project description:This Study sought to understand the differential gene expression profile of Pkd2 mutant mice kidneys in the setting of miR-21 deletion 4 Wild type mice, 3 Pkd2 Knockout mice and 3 Pkd2-miR-21 knockout mice were analyzed

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Next Generation Sequencing of PKD2 mutant mice kidneys

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Project description:ADPKD (Autosomal dominant polycystic kidney disease) is the most common inherited disorders and is characterized by growth of numerous cysts filled with fluid in the kidneys. Ultimately, it leads to kidney failure. The mutations of PKD1 and PKD2 account for approximately 85 and 15 percent of ADPKD, respectively. However, the mechanisms related to genetic mutation of PKD1 and PKD2 are still unclear. To investigate altered gene expression levels, Affymetrix microarray was performed using the kidney tissue from normal and ADPKD patients.

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Mettl3/m6A promotes translation of pathogenic mRNAs to mediate cystogenesis in mouse models of ADPKD

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Next Generation Sequencing Analysis of Prenatal Chlorpyrifos Exposure embryonic kidneys

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Project description:Autosomal dominant polycystic kidney disease (ADPKD) is an important cause of end stage renal disease for which there is no proven therapy 1. Mutations at PKD1 are the principal cause of disease. The disease begins in utero2 and is slowly progressive but it is not known whether cystogenesis is an ongoing process during adult life. We now show that inactivation of Pkd1 in mice prior to post-natal day 13 results in severely cystic kidneys within three weeks, whereas inactivation at day 14 and later results in cysts only after five months. We found that cellular proliferation was not appreciably higher in cystic specimens than in age-matched controls but that the abrupt change in response to Pkd1 inactivation corresponded with a previously unrecognized brake point during renal growth and significant changes in gene expression. These findings suggest that the effects of Pkd1 inactivation are defined by a developmental switch that signals the end of the terminal renal maturation process. These studies show that Pkd1 regulates tubular morphology in both developing and adult kidney but the pathologic consequences of inactivation are defined by the organ’s developmental status, with important clinical implications for our understanding of disease and our approach to therapy. Keywords: Developmental status comparison

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