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DNA methylcytosine dioxygenase ten-eleven translocation 2 enhances lipopolysaccharide-induced cytokine expression in human dental pulp cells by regulating MyD88 hydroxymethylation

Overview of attention for article published in Cell and Tissue Research, April 2018
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Title
DNA methylcytosine dioxygenase ten-eleven translocation 2 enhances lipopolysaccharide-induced cytokine expression in human dental pulp cells by regulating MyD88 hydroxymethylation
Published in
Cell and Tissue Research, April 2018
DOI 10.1007/s00441-018-2826-x
Pubmed ID
Authors

Xinxuan Wang, Zhihui Feng, Qimeng Li, Baicheng Yi, Qiong Xu

Abstract

Dental pulp inflammation is a bacterially driven inflammation process characterized by the local accumulation of cytokines/chemokines that participate in destructive processes in the pulp. Multiple mechanisms are involved in dental pulp inflammation, including epigenetic events, such as DNA methylation/demethylation. Ten-eleven translocation 2 (TET2) is a recently discovered DNA methylcytosine dioxygenase that plays important roles in inflammatory disease. However, its role in the inflammatory response of dental pulp is unknown. We observed elevated mRNA and protein levels of TET2 after lipopolysaccharide (LPS) stimulation in human dental pulp cells (hDPCs). To identify the effects of TET2 on cytokine expression, TET2 was knocked down and cytokines were detected using a cytokine antibody array after LPS stimulation. The protein expression of GM-CSF, IL-6, IL-8 and RANTES decreased in the LPS-induced hDPCs following TET2 knockdown. The downregulated expression levels of IL-6 and IL-8 were further confirmed by real-time quantitative polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA). Additionally, the phosphorylation levels of IKK-α/β, p65 and IκBα of the NF-κB signaling pathway were decreased in the TET2-silenced group. Furthermore, the global 5-hydroxymethylcytosine (5hmC) level was significantly decreased and the genomic 5-methylcytosine (5mC) level was increased in the TET2-deficient hDPCs; TET2 depletion resulted in a decrease in the 5hmC level of the MyD88 promoter following LPS stimulation. These findings indicate that TET2 knockdown inhibits LPS-induced inflammatory response in hDPCs by downregulating MyD88 hydroxymethylation. Thus, TET2-dependent DNA demethylation might play an important role in dental pulp inflammation as an epigenetic regulator.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 17 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 17 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 4 24%
Student > Ph. D. Student 3 18%
Student > Bachelor 3 18%
Librarian 1 6%
Student > Master 1 6%
Other 1 6%
Unknown 4 24%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 5 29%
Medicine and Dentistry 3 18%
Immunology and Microbiology 2 12%
Agricultural and Biological Sciences 1 6%
Social Sciences 1 6%
Other 1 6%
Unknown 4 24%
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 11 July 2019.
All research outputs
#20,105,949
of 24,716,872 outputs
Outputs from Cell and Tissue Research
#1,742
of 2,210 outputs
Outputs of similar age
#260,211
of 332,985 outputs
Outputs of similar age from Cell and Tissue Research
#16
of 19 outputs
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So far Altmetric has tracked 2,210 research outputs from this source. They receive a mean Attention Score of 3.6. This one is in the 13th percentile – i.e., 13% of its peers scored the same or lower than it.
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