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Dcf1 Deficiency Attenuates the Role of Activated Microglia During Neuroinflammation

Overview of attention for article published in Frontiers in Molecular Neuroscience, July 2018
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Title
Dcf1 Deficiency Attenuates the Role of Activated Microglia During Neuroinflammation
Published in
Frontiers in Molecular Neuroscience, July 2018
DOI 10.3389/fnmol.2018.00256
Pubmed ID
Authors

Jiao Wang, Jie Li, Qian Wang, Yanyan Kong, Fangfang Zhou, Qian Li, Weihao Li, Yangyang Sun, Yanli Wang, Yihui Guan, Minghong Wu, Tieqiao Wen

Abstract

Microglia serve as the principal immune cells and play crucial roles in the central nervous system, responding to neuroinflammation via migration and the execution of phagocytosis. Dendritic cell-derived factor 1 (Dcf1) is known to play an important role in neural stem cell differentiation, glioma apoptosis, dendritic spine formation, and Alzheimer's disease (AD), nevertheless, the involvement of the Dcf1 gene in the brain immune response has not yet been reported. In the present paper, the RNA-sequencing and function enrichment analysis suggested that the majority of the down-regulated genes in Dcf1-/- (Dcf1-KO) mice are immune-related. In vivo experiments showed that Dcf1 deletion produced profound effects on microglial function, increased the expression of microglial activation markers, such as ionized calcium binding adaptor molecule 1 (Iba1), Cluster of Differentiation 68 (CD68) and translocator protein (TSPO), as well as certain proinflammatory cytokines (Cxcl1, Ccl7, and IL17D), but decreased the migratory and phagocytic abilities of microglial cells, and reduced the expression levels of some other proinflammatory cytokines (Cox-2, IL-1β, IL-6, TNF-α, and Csf1) in the mouse hippocampus. Furthermore, in vitro experiments revealed that in the absence of lipopolysaccharide (LPS), the majority of microglia were ramified and existed in a resting state, with only approximately 10% of cells exhibiting an amoeboid-like morphology, indicative of an activated state. LPS treatment dramatically increased the ratio of activated to resting cells, and Dcf1 downregulation further increased this ratio. These data indicated that Dcf1 deletion mediates neuroinflammation and induces dysfunction of activated microglia, preventing migration and the execution of phagocytosis. These findings support further investigation into the biological mechanisms underlying microglia-related neuroinflammatory diseases, and the role of Dcf1 in the immune response.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 24 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 24 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 4 17%
Student > Bachelor 4 17%
Student > Ph. D. Student 3 13%
Professor 2 8%
Student > Master 2 8%
Other 4 17%
Unknown 5 21%
Readers by discipline Count As %
Medicine and Dentistry 6 25%
Neuroscience 3 13%
Biochemistry, Genetics and Molecular Biology 2 8%
Agricultural and Biological Sciences 2 8%
Mathematics 1 4%
Other 3 13%
Unknown 7 29%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 2. 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 August 2018.
All research outputs
#15,016,514
of 23,099,576 outputs
Outputs from Frontiers in Molecular Neuroscience
#1,685
of 2,930 outputs
Outputs of similar age
#198,085
of 329,966 outputs
Outputs of similar age from Frontiers in Molecular Neuroscience
#68
of 123 outputs
Altmetric has tracked 23,099,576 research outputs across all sources so far. This one is in the 32nd percentile – i.e., 32% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,930 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.7. This one is in the 36th percentile – i.e., 36% 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 329,966 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 36th percentile – i.e., 36% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 123 others from the same source and published within six weeks on either side of this one. This one is in the 38th percentile – i.e., 38% of its contemporaries scored the same or lower than it.