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September 2012 Volume 6 Issue 3

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Article

ShRNA-mediated gene silencing of AHR promotes the differentiation of P19 mouse embryonic carcinoma cells into cardiomyocytes

  • Authors:
    • Chun Zhu
    • Yu-Lin Chen
    • Xue-Jie Wang
    • Xiao-Shan Hu
    • Zhang-Bin Yu
    • Shu-Ping Han
  • View Affiliations / Copyright

    Affiliations: State Key Laboratory of Reproductive Medicine, Department of Pediatrics, Nanjing Maternity and Child Health Care Hospital Affiliated to Nanjing Medical University, Nanjing 210029, P.R. China , Institute of Pediatrics, Nanjing Medical University, Nanjing 210029, P.R. China
  • Pages: 513-518
    |
    Published online on: June 8, 2012
       https://doi.org/10.3892/mmr.2012.941
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Abstract

The aryl hydrocarbon receptor (AHR) is a basic helix-loop-helix (bHLH) transcription factor that is activated by environmental contaminants including polychlorinated biphenyls (PCBs). The AHR affects a variety of processes that are involved in cell growth and differentiation. In this study, we constructed a P19 embryonic carcinoma cell line with AHR gene silencing using the vector-based approach of short hairpin (sh)RNA interference that allows cells to differentiate into cardiac myocytes when treated with dimethyl sulfoxide (DMSO). The expression levels of the cardiac development-specific GATA4 and Nkx2.5 genes were measured using real-time quantitative polymerase chain reaction (qPCR). Our data showed that the expression levels of the GATA4 and Nkx2.5 genes were increased in the AHR-silenced P19 cells compared with the control groups. Four critical genes (ARNT, CYP1A1, GSK3β and β-catenin) expressed in the AHR and in the Wnt signaling pathway were also measured by qPCR. We found that the expression levels of ARNT, CYP1A1 and β-catenin were suppressed, whereas GSK3β expression was elevated in the AHR-silenced P19 cells. Therefore, it is possible that the silencing of AHR promotes the differentiation of P19 cells through the AHR and Wnt signal transduction pathway.
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Copy and paste a formatted citation
Spandidos Publications style
Zhu C, Chen Y, Wang X, Hu X, Yu Z and Han S: ShRNA-mediated gene silencing of AHR promotes the differentiation of P19 mouse embryonic carcinoma cells into cardiomyocytes. Mol Med Rep 6: 513-518, 2012.
APA
Zhu, C., Chen, Y., Wang, X., Hu, X., Yu, Z., & Han, S. (2012). ShRNA-mediated gene silencing of AHR promotes the differentiation of P19 mouse embryonic carcinoma cells into cardiomyocytes. Molecular Medicine Reports, 6, 513-518. https://doi.org/10.3892/mmr.2012.941
MLA
Zhu, C., Chen, Y., Wang, X., Hu, X., Yu, Z., Han, S."ShRNA-mediated gene silencing of AHR promotes the differentiation of P19 mouse embryonic carcinoma cells into cardiomyocytes". Molecular Medicine Reports 6.3 (2012): 513-518.
Chicago
Zhu, C., Chen, Y., Wang, X., Hu, X., Yu, Z., Han, S."ShRNA-mediated gene silencing of AHR promotes the differentiation of P19 mouse embryonic carcinoma cells into cardiomyocytes". Molecular Medicine Reports 6, no. 3 (2012): 513-518. https://doi.org/10.3892/mmr.2012.941
Copy and paste a formatted citation
x
Spandidos Publications style
Zhu C, Chen Y, Wang X, Hu X, Yu Z and Han S: ShRNA-mediated gene silencing of AHR promotes the differentiation of P19 mouse embryonic carcinoma cells into cardiomyocytes. Mol Med Rep 6: 513-518, 2012.
APA
Zhu, C., Chen, Y., Wang, X., Hu, X., Yu, Z., & Han, S. (2012). ShRNA-mediated gene silencing of AHR promotes the differentiation of P19 mouse embryonic carcinoma cells into cardiomyocytes. Molecular Medicine Reports, 6, 513-518. https://doi.org/10.3892/mmr.2012.941
MLA
Zhu, C., Chen, Y., Wang, X., Hu, X., Yu, Z., Han, S."ShRNA-mediated gene silencing of AHR promotes the differentiation of P19 mouse embryonic carcinoma cells into cardiomyocytes". Molecular Medicine Reports 6.3 (2012): 513-518.
Chicago
Zhu, C., Chen, Y., Wang, X., Hu, X., Yu, Z., Han, S."ShRNA-mediated gene silencing of AHR promotes the differentiation of P19 mouse embryonic carcinoma cells into cardiomyocytes". Molecular Medicine Reports 6, no. 3 (2012): 513-518. https://doi.org/10.3892/mmr.2012.941
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