I. Charalampopoulos, V. I. Alexaki, C. Tsatsanis, V. Minas, E. Dermitzaki, I. Lasaridis, L. Vardouli, C. Stournaras, A. N. Margioris, E. Castanas and A. Gravanis, “Neurosteroids as Endogenous Inhibitors of Neuronal Cell Apoptosis in Aging,” Annals of the New York Academy of Sciences, Vol. 1088, 2006, pp. 139-152. doi:10.1196/annals.1366.003

has been cited by the following article:

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

  AUTHORS: Ping Zou, Chao Qu, Yihui Xu, Hongyan Li, Dannv Han, Dan Shi, Wei Zou

  KEYWORDS: NF-κB; Estrogen Receptor Alpha 36; PC12 Cells

  JOURNAL NAME: Open Journal of Endocrine and Metabolic Diseases, Vol.3 No.4B, August 6, 2013

  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.