Evidence map›Paper›PMID 31209269›Full record

ArticleInternational journal of obesity (2005)2020

Pentraxin 3 deficiency exacerbates lipopolysaccharide-induced inflammation in adipose tissue.

Hong Guo, Xiaoxue Qiu, Jessica Deis, Te-Yueh Lin, Xiaoli Chen

Open access · hybridAbstract read
In one paragraph

Article in International journal of obesity (2005), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 24% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Adipose tissue depot specific expression and regulation of fibrosis-related genes and proteins in experimental obesity.Mammalian genome : official journal of the International Mammalian Genome Society · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
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

5 authors at 1 institution in 1 country.

Hong GuoDepartment of Food Science and Nutrition, University of Minnesota-Twin Cities, St. Paul, MN, 55108, USA.
Xiaoxue QiuDepartment of Food Science and Nutrition, University of Minnesota-Twin Cities, St. Paul, MN, 55108, USA.
Jessica DeisDepartment of Food Science and Nutrition, University of Minnesota-Twin Cities, St. Paul, MN, 55108, USA.
Te-Yueh LinDepartment of Food Science and Nutrition, University of Minnesota-Twin Cities, St. Paul, MN, 55108, USA.
Xiaoli ChenDepartment of Food Science and Nutrition, University of Minnesota-Twin Cities, St. Paul, MN, 55108, USA. xlchen@umn.edu.
University of Minnesota · US

Funding

Women's CancerP30CA077598 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI HEATHER Hammond NELSON · 1998 to 2026
$100.4M
NCI NIH HHS P30 CA077598
6 · The paper itself

Abstract

BACKGROUND/

objectivesPentraxin 3 (PTX3) has been characterized as a soluble and multifunctional pattern recognition protein in the regulation of innate immune response. However, little is known about its role in adipose tissue inflammation and obesity. Herein, we investigated the role of PTX3 in the regulation of lipopolysaccharide (LPS)-induced inflammation in adipocytes and adipose tissue, as well as high-fat diet (HFD)-induced metabolic inflammation in obesity.

methodsPtx3 knockdown 3T3-L1 Cells were generated using shRNA for Ptx3 gene and treated with different inflammatory stimuli. For the in vivo studies, Ptx3 knockout mice were treated with 0.3 mg/kg of LPS for 6 h. Adipose tissues were collected for gene and protein expression by qPCR and western blotting, respectively. Ptx3 knockout mice were fed with HFD for 12 week since 6 week of age.

resultsWe observed that the expression of PTX3 in adipose tissue and serum PTX3 were markedly increased in response to LPS administration. Knocking down Ptx3 in 3T3-L1 cells reduced adipogenesis and caused a more profound and sustained upregulation of proinflammatory gene expression and signaling pathway activation during LPS-stimulated inflammation in 3T3-L1 adipocytes. In vivo studies showed that PTX3 deficiency significantly exacerbated the LPS-induced upregulation of inflammatory genes and downregulation of adipogeneic genes in visceral and subcutaneous adipose tissue of mice. Accordingly, LPS stimulation elicited increased activation of nuclear factor-κB (NF-κB) and p44/42 MAPK (Erk1/2) signaling pathways in visceral and subcutaneous adipose tissue. The expression of PTX3 in adipose tissue was also induced by HFD, and PTX3 deficiency led to the upregulation of proinflammatory genes in visceral adipose tissue of HFD-induced obese mice.

conclusionsOur results suggest a protective role of PTX3 in LPS- and HFD-induced sustained inflammation in adipose tissue.

Indexed as

C-Reactive ProteinNerve Tissue Proteins3T3-L1 CellsAdipose TissueAnimalsDiet, High-FatFemaleInflammationLipopolysaccharidesMaleMiceMice, Inbred C57BLMice, KnockoutMice, ObesePentraxinsC-Reactive ProteinLipopolysaccharidesNerve Tissue ProteinsPentraxins

Identifiers

PMID31209269
PMCPMC6997122
OpenAlexW2951424272

What OpenQuestion 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 OpenQuestion graph.