↓ Skip to main content

NOD2 promotes dopaminergic degeneration regulated by NADPH oxidase 2 in 6-hydroxydopamine model of Parkinson’s disease

Overview of attention for article published in Journal of Neuroinflammation, August 2018
Altmetric Badge

Mentioned by

twitter
1 X user
facebook
1 Facebook page

Citations

dimensions_citation
37 Dimensions

Readers on

mendeley
49 Mendeley
You are seeing a free-to-access but limited selection of the activity Altmetric has collected about this research output. Click here to find out more.
Title
NOD2 promotes dopaminergic degeneration regulated by NADPH oxidase 2 in 6-hydroxydopamine model of Parkinson’s disease
Published in
Journal of Neuroinflammation, August 2018
DOI 10.1186/s12974-018-1289-z
Pubmed ID
Authors

Li Cheng, Lin Chen, Xinbing Wei, Yimeng Wang, Zhiping Ren, Shenglan Zeng, Xiumei Zhang, Haitao Wen, Chengjiang Gao, Huiqing Liu

Abstract

In Parkinson's disease (PD), loss of striatal dopaminergic (DA) terminals and degeneration of DA neurons in the substantia nigra (SN) are associated with inflammation. Nucleotide-binding oligomerization domain-containing protein (NOD)2, one of the first discovered NOD-like receptors, plays an important role in inflammation. However, the role of NOD2 has not been elucidated in PD. NOD2 mRNA and protein expression in the SN and the striatum of C57BL/6 mice treated with 6-hydroxydopamine (6-OHDA) was measured. We next investigated the potential contribution of the NOD2-dependent pathway to 6-OHDA-induced DA degeneration using NOD2-deficient (NOD2-/-) mice. Assays examining DA degeneration and inflammation include HPLC, Western blot, immunohistochemistry, TUNEL staining, and cytometric bead array. To further explore a possible link between NADPH oxidase 2 (NOX2) and NOD2 signaling in PD, microglia were transfected with shRNA specific to NOX2 in vitro and apocynin were given to mice subjected to 6-OHDA and muramyl dipeptide (MDP) striatal injection. The expression of NOD2 was upregulated in an experimental PD model induced by the neurotoxin 6-OHDA. NOD2 deficiency resulted in a protective effect against 6-OHDA-induced DA degeneration and neuronal death, which was associated with the attenuated inflammatory response. Moreover, silencing of NOX2 in microglia suppressed the expression of NOD2 and the inflammatory response induced by 6-OHDA and attenuated the toxicity of conditioned medium from 6-OHDA or MDP-stimulated microglia to neuronal cells. Furthermore, apocynin treatment inhibited NOD2 upregulation and DA degeneration in the SN of WT mice induced by 6-OHDA and MDP. This study provides the direct evidence that NOD2 is related to 6-OHDA-induced DA degeneration through NOX2-mediated oxidative stress, indicating NOD2 is a novel innate immune signaling molecule participating in PD inflammatory response.

X Demographics

X Demographics

The data shown below were collected from the profile of 1 X user who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 49 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 49 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 11 22%
Student > Master 4 8%
Student > Doctoral Student 4 8%
Professor 3 6%
Student > Bachelor 3 6%
Other 8 16%
Unknown 16 33%
Readers by discipline Count As %
Neuroscience 6 12%
Biochemistry, Genetics and Molecular Biology 5 10%
Medicine and Dentistry 5 10%
Engineering 3 6%
Psychology 2 4%
Other 9 18%
Unknown 19 39%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 16 April 2019.
All research outputs
#18,648,325
of 23,102,082 outputs
Outputs from Journal of Neuroinflammation
#2,092
of 2,662 outputs
Outputs of similar age
#257,504
of 335,220 outputs
Outputs of similar age from Journal of Neuroinflammation
#48
of 63 outputs
Altmetric has tracked 23,102,082 research outputs across all sources so far. This one is in the 11th percentile – i.e., 11% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,662 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 7.6. This one is in the 12th percentile – i.e., 12% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 335,220 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 12th percentile – i.e., 12% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 63 others from the same source and published within six weeks on either side of this one. This one is in the 14th percentile – i.e., 14% of its contemporaries scored the same or lower than it.