TY - JOUR
T1 - Protective microglia and their regulation in Parkinson’s disease
AU - Le, Weidong
AU - Wu, Junjiao
AU - Tang, Yu
N1 - Funding Information:
This work was supported by grants from the National Natural Sciences Foundation of China (No. 81430021 and 81370470), the Program for Liaoning Innovative Research Team in University (LT2015009), and Liaoning Science and Technology Project (2015225008).
Publisher Copyright:
© 2016 Le, Wu and Tang.
PY - 2016/9/21
Y1 - 2016/9/21
N2 - Microglia-mediated neuroinflammation is a hallmark of Parkinson’s disease (PD). In the brains of patients with PD, microglia have both neurotoxic and neuroprotective effects, depending on their activation state. In this review, we focus on recent research demonstrating the neuroprotective role of microglia in PD. Accumulating evidence indicates that the protective mechanisms of microglia may result from their regulation of transrepression pathways via nuclear receptors, anti-inflammatory responses, neuron-microglia crosstalk, histone modification, and microRNA regulation. All of these mechanisms work together to suppress the production of neurotoxic inflammatory components. However, during the progression of PD, the detrimental effects of inflammation overpower the protective actions of microglia. Therefore, an in-depth exploration of the mechanisms underlying microglial neuroprotection, and a means of promoting the transformation of microglia to the protective phenotype, are urgently needed for the treatment of PD.
AB - Microglia-mediated neuroinflammation is a hallmark of Parkinson’s disease (PD). In the brains of patients with PD, microglia have both neurotoxic and neuroprotective effects, depending on their activation state. In this review, we focus on recent research demonstrating the neuroprotective role of microglia in PD. Accumulating evidence indicates that the protective mechanisms of microglia may result from their regulation of transrepression pathways via nuclear receptors, anti-inflammatory responses, neuron-microglia crosstalk, histone modification, and microRNA regulation. All of these mechanisms work together to suppress the production of neurotoxic inflammatory components. However, during the progression of PD, the detrimental effects of inflammation overpower the protective actions of microglia. Therefore, an in-depth exploration of the mechanisms underlying microglial neuroprotection, and a means of promoting the transformation of microglia to the protective phenotype, are urgently needed for the treatment of PD.
KW - Alternative activation
KW - Anti-inflammation
KW - Histone modification
KW - MicroRNA
KW - Neuroinflammation
KW - Parkinson’s disease
KW - Transrepression pathway
UR - http://www.scopus.com/inward/record.url?scp=84989844583&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84989844583&partnerID=8YFLogxK
U2 - 10.3389/fnmol.2016.00089
DO - 10.3389/fnmol.2016.00089
M3 - Review article
AN - SCOPUS:84989844583
SN - 1662-5099
VL - 9
JO - Frontiers in Molecular Neuroscience
JF - Frontiers in Molecular Neuroscience
IS - SEP2016
M1 - 89
ER -