锰通过激活 ERK 诱导 PC12 细胞中 α-突触核蛋白的过度表达。
Manganese induces the overexpression of α-synuclein in PC12 cells via ERK activation.
机构信息
Department of Occupational and Environmental Health, School of Public Health, Fourth Military Medical University, Xi'an 710032, China.
出版信息
Brain Res. 2010 Nov 4;1359:201-7. doi: 10.1016/j.brainres.2010.08.055. Epub 2010 Aug 22.
Manganese has been known to induce neurological disorders. In the present study, we determined the effect of manganese on the expression of α-synuclein in PC12 cells and its role in manganese-induced cytotoxicity. We also investigated the relationship between α-synuclein expression and the change of ERK1/2 MAPK activity. In our research, manganese exposure induced the overexpression of α-synuclein, while siRNA knockdown of α-synuclein reversed manganese-induced cytotoxicity. Furthermore, manganese induced the activation of ERK1/2 MAPK. The MEK1 inhibitor PD98059, which inhibits the activation of ERK MAPK, attenuated the overexpression of α-synuclein and the cytotoxicity induced by manganese. In conclusion, our studies show that manganese may induce the overexpression of α-synuclein via ERK1/2 activation, which may play a role in manganese-induced cytotoxicity.
锰已被证实会诱发神经紊乱。在本研究中，我们测定了锰对 PC12 细胞中α-突触核蛋白表达的影响，以及其在锰诱导的细胞毒性中的作用。我们还研究了α-突触核蛋白表达与 ERK1/2 MAPK 活性变化之间的关系。在我们的研究中，锰暴露诱导了α-突触核蛋白的过表达，而α-突触核蛋白的 siRNA 敲低逆转了锰诱导的细胞毒性。此外，锰诱导了 ERK1/2 MAPK 的激活。MEK1 抑制剂 PD98059 抑制 ERK MAPK 的激活，减弱了锰诱导的α-突触核蛋白过表达和细胞毒性。总之，我们的研究表明，锰可能通过 ERK1/2 的激活诱导α-突触核蛋白的过表达，这可能在锰诱导的细胞毒性中发挥作用。
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