期刊
INTERNATIONAL JOURNAL OF NEUROSCIENCE
卷 123, 期 10, 页码 705-710出版社
INFORMA HEALTHCARE
DOI: 10.3109/00207454.2013.795149
关键词
glial cell line-derived neurotrophic factor; 6-hydroxydopamine; nuclear factor (NF)-kappa B (p65/p52); MN9D cell; Bcl-2; Bcl-w; Bax; Bad
资金
- National Natural Science Research Funds of China [30900417, 30901402]
- Natural science Funds for Colleges and Universities in Jiangsu Province [08KJB180011, 09KJD320008]
Glial-cell-line-derived neurotrophic factor (GDNF) has been shown to protect dopaminergic (DA) neurons against 6-hydroxydopamine (6-OHDA) toxicity. The mechanism underlying the antiapoptosis role of GDNF still needs further studies. We previously observed that nuclear factor-kappaB (NF-kappa B) signaling pathway, i.e. p65/p52, mediated the antiapoptosis role of GDNF in MN9D cells. Here, the DA cell line MN9D was used to explore the mechanisms underlying NF-kappa B p65/p52-mediated protection role of GDNF in DA neurons. The results showed that GDNF pretreatment blocked the apoptotic effects induced by 6-OHDA, with the upregulation of the antiapoptotic protein, Bcl-2 and Bcl-w, as well as the downregulation of the proapoptotic proteins, Bax and Bad. Furthermore, when sip100 plasmids were transfected into MN9D cells to inhibit the expression of p100, which was the precursor of p52, the effects of GDNF on upregulating Bcl-2 and Bcl-w were attenuated. These results indicated that GDNF could protect MN9D cells from apoptosis induced by 6-OHDA via upregulating Bcl-2 and Bcl-w expressions and downregulating Box and Bad expressions. Moreover, NF-kappa B p65/p52 signaling mediated the effects of GDNF on Bcl-2 and Bcl-w expressions.
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