Evidence map›Paper›PMID 28634844›Full record

ArticleInflammation2017

Thrombospondin-1 Production Regulates the Inflammatory Cytokine Secretion in THP-1 Cells Through NF-κB Signaling Pathway.

Tian Xing, Yao Wang, Wen-Jie Ding, Yuan-Ling Li, Xiao-Dong Hu, Cong Wang, Ao Ding, Ji-Long Shen

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 31 citations in OpenAlex.

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  4. CD47 and thrombospondin-1 contribute to immune evasion byProceedings of the National Academy of Sciences of the United States of America · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Tian XingDepartment of Immunology, Anhui Medical University, Hefei, 230022, China.
Yao WangDepartment of Pathogen Biology, Provincial Laboratories of Pathogen Biology and Zoonoses, Hefei, Anhui, 230022, China.
Wen-Jie DingDepartment of Pathogen Biology, Provincial Laboratories of Pathogen Biology and Zoonoses, Hefei, Anhui, 230022, China.
Yuan-Ling LiDepartment of Pathogen Biology, Provincial Laboratories of Pathogen Biology and Zoonoses, Hefei, Anhui, 230022, China.
Xiao-Dong HuDepartment of Pathogen Biology, Provincial Laboratories of Pathogen Biology and Zoonoses, Hefei, Anhui, 230022, China.
Cong WangDepartment of Pathogen Biology, Provincial Laboratories of Pathogen Biology and Zoonoses, Hefei, Anhui, 230022, China.
Ao DingStomatology Department of Affiliated Provincial Hospital, Anhui Medical University, Hefei, 230001, China.
Ji-Long ShenDepartment of Immunology, Anhui Medical University, Hefei, 230022, China. shenjilong53@126.com.
Anhui Medical University · CN

Funding

National Natural Science Foundation of China 81600845
6 · The paper itself

Abstract

Thrombospondin-1 (TSP-1) is upregulated in several inflammatory diseases. Recent data have shown that macrophages from TSP-1-deficient mice have a reduced inflammatory phenotype, suggesting that TSP-1 plays a part in macrophage activation. DNA microarray approach revealed that Porphyromonas gingivalis lipopolysaccharide (P. gingivalis LPS) may induce the enhanced TSP-1 expression in human monocytes, suggesting a role of TSP-1-mediated pathogenesis in periodontitis. Until recently, the function of TSP-1 has been a matter of debate. In this study, we explored the role of TSP-1 in inflammatory cytokine secretions and its putative mechanism in pathogenesis of periodontitis. We demonstrated that TSP-1 expression was significantly upregulated in gingival tissues with periodontitis and in P. gingivalis LPS-stimulated THP-1 cells. Deficiency of TSP-1 by transfecting siRNAs decreased IL-6, IL-1β, and TNF-α secretions in THP-1 cells, whereas overexpression of TSP-1 resulted in an upregulation of IL-6, IL-1β, and TNF-α productions. Additional experiments showed that Pyrrolidine dithiocarbamate (PDTC) inhibited IL-6, IL-1β, and TNF-α expression induced by overexpression of TSP-1, accompanying with downregulation of phosphorylated p65 and IκBα protein levels in response to P. gingivalis LPS. These results indicated that TSP-1 played a significant role in P. gingivalis LPS-initiated inflammatory cytokines (IL-6, IL-1β, and TNF-α) secretions of THP-1 cells, and the NF-κB signaling is involved in its induction of expression. Thus, TSP-1 effectively elevated P. gingivalis LPS-induced inflammation mediated by the NF-κB pathway and may be critical for pathology of periodontitis.

Indexed as

CytokinesHumansInflammationLipopolysaccharidesNF-kappa BPeriodontitisPorphyromonas gingivalisSignal TransductionTHP-1 CellsThrombospondin 1CytokinesLipopolysaccharidesNF-kappa BThrombospondin 1thrombospondin-1, humanIL-1βIL-6NF-κB signalingPDTCP. gingivalis LPSTNF-αTSP-1

Identifiers

PMID28634844
OpenAlexW2633522604

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.