Evidence map›Paper›PMID 27246393›Full record

ArticleScientific reports2016

Endogenous sulfur dioxide is a novel adipocyte-derived inflammatory inhibitor.

Heng Zhang, Yaqian Huang, Dingfang Bu, Selena Chen, Chaoshu Tang, Guang Wang, Junbao Du, Hongfang Jin

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
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  5. Review
  6. Role of Militarine in PMNeurochemical research · 2021
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  7. Endogenous SORedox biology · 2021
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  8. Effect of sulfur dioxide on vascular biology.Histology and histopathology · 2021
    Review
  9. Endothelial Cell-Derived SOOxidative medicine and cellular longevity · 2021
    Article
  10. Article
  11. PPARMediators of inflammation · 2019
    Article
  12. Article
  13. Perivascular adipose tissue: epiphenomenon or local risk factor?International journal of obesity (2005) · 2017
    Review
  14. Article
  15. Review
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 5 institutions in 2 countries.

Heng ZhangDepartment of Endocrinology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Yaqian HuangDepartment of Pediatrics, Peking University First Hospital, Beijing 100034, China.
Dingfang BuResearch Center, Peking University First Hospital, Beijing 100034, China.
Selena ChenUniversity of California, San Diego, La Jolla, California, 92093, United States of America.
Chaoshu TangDepartment of Physiology and Pathophysiology, Peking University Health Science Center, Beijing 100191, China.
Guang WangDepartment of Endocrinology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Junbao DuDepartment of Pediatrics, Peking University First Hospital, Beijing 100034, China.
Hongfang JinDepartment of Pediatrics, Peking University First Hospital, Beijing 100034, China.
Peking University · CNCapital Medical University · CNMinistry of Education of the People's Republic of China · CNPeking University First Hospital · CNUniversity of California, San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study was designed to determine whether sulfur dioxide (SO2) could be endogenously produced in adipocyte and served as a novel adipocyte-derived inflammatory inhibitor. SO2 was detected in adipose tissue using high-performance liquid chromatography with fluorescence detection. SO2 synthase aspartate aminotransferase (AAT1 and AAT2) mRNA and protein expressions in adipose tissues were measured. For in vitro study, 3T3-L1 adipocytes were cultured, infected with adenovirus carrying AAT1 gene or lentivirus carrying shRNA to AAT1, and then treated with tumor necrosis factor-α (TNF-α). We found that endogenous SO2/AAT pathway existed in adipose tissues including perivascular, perirenal, epididymal, subcutaneous and brown adipose tissue. AAT1 overexpression significantly increased SO2 production and inhibited TNF-α-induced inflammatory factors, monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8) secretion from 3T3-L1 adipocytes. By contrast, AAT1 knockdown decreased SO2 production and exacerbated TNF-α-stimulated MCP-1 and IL-8 secretion. Mechanistically, AAT1 overexpression attenuated TNF-α-induced IκBα phosphorylation and degradation, and nuclear factor-κB (NF-κB) p65 phosphorylation, while AAT1 knockdown aggravated TNF-α-activated NF-κB pathway, which was blocked by SO2. NF-κB inhibitors, PDTC or Bay 11-7082, abolished excessive p65 phosphorylation and adipocyte inflammation induced by AAT1 knockdown. This is the first report to suggest that endogenous SO2 is a novel adipocyte-derived inflammatory inhibitor.

Indexed as

3T3-L1 CellsAdipocytesAdipose Tissue, BrownAdipose Tissue, WhiteAnimalsAnti-Inflammatory AgentsAspartate AminotransferasesChemokine CCL2Gene Expression RegulationInterleukin-8IsoenzymesMaleMiceNF-KappaB Inhibitor alphaNitrilesPhosphorylation3-(4-methylphenylsulfonyl)-2-propenenitrileAnti-Inflammatory AgentsAspartate AminotransferasesCcl2 protein, mouseChemokine CCL2Interleukin-8IsoenzymesNF-KappaB Inhibitor alphaNitrilesProlineprolinedithiocarbamateRela protein, mouseRNA, Small InterferingSulfonesSulfur DioxideThiocarbamatesTranscription Factor RelATumor Necrosis Factor-alpha

Identifiers

PMID27246393
PMCPMC4887903
OpenAlexW2428622733

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.