Abstract：
:Chronic manganese (Mn) exposure can lead to neuroinflammation and neurological deficit, which resemble idiopathic Parkinson's disease (IPD). However, the precise mechanisms underlying Mn exposure-induced neurotoxicity remain incompletely understood. Microglia can become hyperactivated and plays a vital role in neuroinflammation and consequent neurodegeneration in response to pro-inflammatory stimuli. In the present study, we found that HAPI microglial cells exhibited increased secretion of pro-inflammatory TNF-α and IL-1β following Mn exposure in dose- and time-dependent manners. In addition, we showed that Mn exposure could trigger the activation of JAK2/STAT3 signaling pathway in microglia. Notably, Mn-induced secretion of TNF-α and IL-1β was significantly attenuated by the treatment of JAK2 inhibitor. Finally, through incubating PC12 neuronal cells with Mn-treated microglial conditioned medium, we demonstrated that Mn-induced secretion of microglial TNF-α and IL-1β facilitated neuronal apoptosis. Thus, we speculate that Mn exposure might trigger JAK2-STAT3 signal pathway in microglia, leading to resultant neuroinflammation and neuronal loss.
journal_name
Neurotoxicologyjournal_title
Neurotoxicologyauthors
Yin L,Dai Q,Jiang P,Zhu L,Dai H,Yao Z,Liu H,Ma X,Qu L,Jiang Jdoi
10.1016/j.neuro.2017.04.001subject
Has Abstractpub_date
2018-01-01 00:00:00pages
195-203eissn
0161-813Xissn
1872-9711pii
S0161-813X(17)30060-8journal_volume
64pub_type
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