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Estrogen Receptor Alpha 36 Gene Knockdown Promote the Expression of NF-κB in PC12 Cells

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DOI: 10.4236/ojemd.2013.34A2003    2,564 Downloads   4,294 Views   Citations

ABSTRACT

The nuclear transcription factors κB (NF-κB) is widely existing in various kinds of cell types in the nervous system and plays an important role in neuron apoptosis and neurodegenerative diseases. Estrogen receptor alpha 36 (ER-α36), is a novel variant of ERα (as known ER-α66) which can transduce both estrogenand antiestrogen-dependent activation of MAPK signal pathway and stimulate cell growth. Here, we aimed to detect the effect of ER-α36 gene silencing on the expression of NF-κB in normal cultured PC12 cells and to provide an experimental foundation for understanding the function of ER-α36 innerve cells. PC12 cells with ER-α36 expression knocked down by the shRNA method. Then Western blot and immunocytochemical staining were performed to detect the expression and translocation of NF-κB after transfection. The results showed that NF-κB expression was significantly higher comparing with the control group after transfection (P < 0.01). Also, NF-κB subunit entered nuclear after transfection; Immunofluorescence staining and immunocytochemical staining of PC12 cells demonstrated that ER-α36 was expressed mainly on the plasma membrane and on the cell nucleus membrane. These data indicate that ER-α36 gene silencing can increase the expression of NF-κB and promote its nuclear translocation in PC12 cells.

Conflicts of Interest

The authors declare no conflicts of interest.

Cite this paper

P. Zou, C. Qu, Y. Xu, H. Li, D. Han, D. Shi and W. Zou, "Estrogen Receptor Alpha 36 Gene Knockdown Promote the Expression of NF-κB in PC12 Cells," Open Journal of Endocrine and Metabolic Diseases, Vol. 3 No. 4B, 2013, pp. 20-24. doi: 10.4236/ojemd.2013.34A2003.

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