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Differential Expression of PKD2-Associated Genes in Autosomal Dominant Polycystic Kidney Disease.

Yook YJ, Woo YM, Yang MH, Ko JY, Kim BH, Lee EJ, Chang ES, Lee MJ, Lee S, Park JH - Genomics Inform (2012)

Bottom Line: Autosomal dominant polycystic kidney disease (ADPKD) is characterized by formation of multiple fluid-filled cysts that expand over time and destroy renal architecture.The majority of identified mutations was involved in critical biological processes, such as metabolism, transcription, cell adhesion, cell cycle, and signal transduction.These data may be helpful in PKD2-related mechanisms of ADPKD pathogenesis.

View Article: PubMed Central - PubMed

Affiliation: Department of Biological Science, Sookmyung Women's University, Seoul 140-742, Korea.

ABSTRACT
Autosomal dominant polycystic kidney disease (ADPKD) is characterized by formation of multiple fluid-filled cysts that expand over time and destroy renal architecture. The proteins encoded by the PKD1 and PKD2 genes, mutations in which account for nearly all cases of ADPKD, may help guard against cystogenesis. Previously developed mouse models of PKD1 and PKD2 demonstrated an embryonic lethal phenotype and massive cyst formation in the kidney, indicating that PKD1 and PKD2 probably play important roles during normal renal tubular development. However, their precise role in development and the cellular mechanisms of cyst formation induced by PKD1 and PKD2 mutations are not fully understood. To address this question, we presently created Pkd2 knockout and PKD2 transgenic mouse embryo fibroblasts. We used a mouse oligonucleotide microarray to identify messenger RNAs whose expression was altered by the overexpression of the PKD2 or knockout of the Pkd2. The majority of identified mutations was involved in critical biological processes, such as metabolism, transcription, cell adhesion, cell cycle, and signal transduction. Herein, we confirmed differential expressions of several genes including aquaporin-1, according to different PKD2 expression levels in ADPKD mouse models, through microarray analysis. These data may be helpful in PKD2-related mechanisms of ADPKD pathogenesis.

No MeSH data available.


Related in: MedlinePlus

Establishment of Pkd2 KO and PKD2 TG MEFs. (A) Semi-quantitative reverse transcription-PCR analysis of Pkd2 gene in Pkd2 KO and PKD2 TG MEF cells. Human- or mouse-specific PKD2 primer sets were used. 18s rRNA was used as a loading control. (B) Western blot analysis of polycystin 2 (PC2) expression in Pkd2 KO and PKD2 TG MEF cells. MEFs, mouse embryo fibroblasts; KO, knockout (MEF); TG, transgenic (MEF); KOWT, knockout wild-type (MEF); TGWT, transgenic wild-type (MEF).
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Figure 1: Establishment of Pkd2 KO and PKD2 TG MEFs. (A) Semi-quantitative reverse transcription-PCR analysis of Pkd2 gene in Pkd2 KO and PKD2 TG MEF cells. Human- or mouse-specific PKD2 primer sets were used. 18s rRNA was used as a loading control. (B) Western blot analysis of polycystin 2 (PC2) expression in Pkd2 KO and PKD2 TG MEF cells. MEFs, mouse embryo fibroblasts; KO, knockout (MEF); TG, transgenic (MEF); KOWT, knockout wild-type (MEF); TGWT, transgenic wild-type (MEF).

Mentions: Mouse Pkd2 mRNA was revealed in KO wild-type (KOWT) MEF cells but not in KO MEF cells. Also, Pkd2 mRNA was expressed in TG wild-type (TGWT) MEF cells and PKD2 TG MEF cells. Human PKD2 mRNA was only expressed in PKD2 TG MEF cells obtained from PKD2 TG embryos following injection of the human PKD2 transgene (Fig. 1A). Consistently, the expression level of polycystin-2 was lower in KO MEFs than KOWT MEFs as well as higher in TG MEFs than TGWT MEFs (Fig. 1B).


Differential Expression of PKD2-Associated Genes in Autosomal Dominant Polycystic Kidney Disease.

Yook YJ, Woo YM, Yang MH, Ko JY, Kim BH, Lee EJ, Chang ES, Lee MJ, Lee S, Park JH - Genomics Inform (2012)

Establishment of Pkd2 KO and PKD2 TG MEFs. (A) Semi-quantitative reverse transcription-PCR analysis of Pkd2 gene in Pkd2 KO and PKD2 TG MEF cells. Human- or mouse-specific PKD2 primer sets were used. 18s rRNA was used as a loading control. (B) Western blot analysis of polycystin 2 (PC2) expression in Pkd2 KO and PKD2 TG MEF cells. MEFs, mouse embryo fibroblasts; KO, knockout (MEF); TG, transgenic (MEF); KOWT, knockout wild-type (MEF); TGWT, transgenic wild-type (MEF).
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC3475485&req=5

Figure 1: Establishment of Pkd2 KO and PKD2 TG MEFs. (A) Semi-quantitative reverse transcription-PCR analysis of Pkd2 gene in Pkd2 KO and PKD2 TG MEF cells. Human- or mouse-specific PKD2 primer sets were used. 18s rRNA was used as a loading control. (B) Western blot analysis of polycystin 2 (PC2) expression in Pkd2 KO and PKD2 TG MEF cells. MEFs, mouse embryo fibroblasts; KO, knockout (MEF); TG, transgenic (MEF); KOWT, knockout wild-type (MEF); TGWT, transgenic wild-type (MEF).
Mentions: Mouse Pkd2 mRNA was revealed in KO wild-type (KOWT) MEF cells but not in KO MEF cells. Also, Pkd2 mRNA was expressed in TG wild-type (TGWT) MEF cells and PKD2 TG MEF cells. Human PKD2 mRNA was only expressed in PKD2 TG MEF cells obtained from PKD2 TG embryos following injection of the human PKD2 transgene (Fig. 1A). Consistently, the expression level of polycystin-2 was lower in KO MEFs than KOWT MEFs as well as higher in TG MEFs than TGWT MEFs (Fig. 1B).

Bottom Line: Autosomal dominant polycystic kidney disease (ADPKD) is characterized by formation of multiple fluid-filled cysts that expand over time and destroy renal architecture.The majority of identified mutations was involved in critical biological processes, such as metabolism, transcription, cell adhesion, cell cycle, and signal transduction.These data may be helpful in PKD2-related mechanisms of ADPKD pathogenesis.

View Article: PubMed Central - PubMed

Affiliation: Department of Biological Science, Sookmyung Women's University, Seoul 140-742, Korea.

ABSTRACT
Autosomal dominant polycystic kidney disease (ADPKD) is characterized by formation of multiple fluid-filled cysts that expand over time and destroy renal architecture. The proteins encoded by the PKD1 and PKD2 genes, mutations in which account for nearly all cases of ADPKD, may help guard against cystogenesis. Previously developed mouse models of PKD1 and PKD2 demonstrated an embryonic lethal phenotype and massive cyst formation in the kidney, indicating that PKD1 and PKD2 probably play important roles during normal renal tubular development. However, their precise role in development and the cellular mechanisms of cyst formation induced by PKD1 and PKD2 mutations are not fully understood. To address this question, we presently created Pkd2 knockout and PKD2 transgenic mouse embryo fibroblasts. We used a mouse oligonucleotide microarray to identify messenger RNAs whose expression was altered by the overexpression of the PKD2 or knockout of the Pkd2. The majority of identified mutations was involved in critical biological processes, such as metabolism, transcription, cell adhesion, cell cycle, and signal transduction. Herein, we confirmed differential expressions of several genes including aquaporin-1, according to different PKD2 expression levels in ADPKD mouse models, through microarray analysis. These data may be helpful in PKD2-related mechanisms of ADPKD pathogenesis.

No MeSH data available.


Related in: MedlinePlus