https://www.ncbi.nlm.nih.gov/pubmed/31831012?dopt=Abstract
TITLE:
CXCL12 is involved in α-synuclein-triggered neuroinflammation of Parkinson’s disease.
DESCRIPTION:
Related Articles
CXCL12 is involved in α-synuclein-triggered neuroinflammation of Parkinson’s disease.
J Neuroinflammation. 2019 Dec 12;16(1):263
Authors: Li Y, Niu M, Zhao A, Kang W, Chen Z, Luo N, Zhou L, Zhu X, Lu L, Liu J
Abstract
BACKGROUND: The mechanisms underlying the pathogenesis and progression of Parkinson’s disease (PD) remain elusive, but recent opinions and perspectives have focused on whether the inflammation process induced by microglia contributes to α-synuclein-mediated toxicity. Migration of microglia to the substantia nigra (SN) could precede neurodegeneration in A53T mice. We hypothesized that CXCL12 could be a mediator in the α-synuclein-induced migration of microglia.
METHODS: After establishing appropriate animal and cell culture models, we explored the relationship between α-synuclein and CXCL12 in A53T mice, primary microglia, and BV-2 cell lines. We also explored the mechanisms of these interactions and the signaling processes involved in neuroinflammation.
RESULTS: We confirmed the positive correlation between α-synuclein and CXCL12 in the postmortem brain tissue of PD patients and the upregulated CXCR4 expression in SN microglia of A53T mice. In addition, as expected, α-synuclein increased the production of CXCL12 in microglia via TLR4/IκB-α/NF-κB signaling. Importantly, CXCL12/CXCR4/FAK/Src/Rac1 signaling was shown to be involved in α-synuclein-induced microglial accumulation.
CONCLUSIONS: Our study suggests that CXCL12 could be a novel target for the prevention of α-synuclein-triggered ongoing microglial responses. Blocking CXCL12/CXCR4 may be a potential therapeutic approach for PD progression.
PMID: 31831012 [PubMed – in process]
PMID:
PubMed:31831012
DATE FOUND:
12/14/19 06:02AM
LINK / URL:
https://www.ncbi.nlm.nih.gov/pubmed/31831012?dopt=Abstract
