Evidence map›Paper›PMID 23227233›Full record

ArticlePloS one2012

Elastase and tryptase govern TNFα-mediated production of active chemerin by adipocytes.

Sebastian D Parlee, Jenna O McNeil, Shanmugam Muruganandan, Christopher J Sinal, Kerry B Goralski

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. CHEMERIN AND FACTORS RELATED TO CARDIOVASCULAR RISK IN CHILDREN AND ADOLESCENTS: A SYSTEMATIC REVIEW.Revista paulista de pediatria : orgao oficial da Sociedade de Pediatria de Sao Paulo
    Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Chemerin regulates formation and function of brown adipose tissue: Ablation results in increased insulin resistance with high fat challenge and aging.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  13. Review
  14. Chemerin as a Driver of Hypertension: A Consideration.American journal of hypertension · 2020
    Review
  15. Review
  16. Article
  17. Chemerin promotes angiogenesis in vivo.Physiological reports · 2018
    Article
  18. Article
  19. Article
  20. 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.

Sebastian D ParleeDepartment of Pharmacology, Dalhousie University, Halifax, Nova Scotia, Canada.
Jenna O McNeil
Shanmugam Muruganandan
Christopher J Sinal
Kerry B Goralski
Dalhousie University · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Chemerin is a leukocyte chemoattractant and adipokine with important immune and metabolic roles. Chemerin, secreted in an inactive form prochemerin, undergoes C-terminal proteolytic cleavage to generate active chemerin, a ligand for the chemokine-like receptor-1 (CMKLR1). We previously identified that adipocytes secrete and activate chemerin. Following treatment with the obesity-associated inflammatory mediator TNFα, unknown adipocyte mechanisms are altered resulting in an increased ratio of active to total chemerin production. Based on these findings we hypothesized adipocytes produce proteases capable of modifying chemerin and its ability to activate CMKRL1. 3T3-L1 adipocytes expressed mRNA of immunocyte and fibrinolytic proteases known to activate chemerin in vitro. Following treatment with a general protease inhibitor cocktail (PIC), the TNFα-stimulated increase in apparent active chemerin concentration in adipocyte media was amplified 10-fold, as measured by CMKLR1 activation. When the components of the PIC were investigated individually, aprotinin, a serine protease inhibitor, blocked 90% of the TNFα-associated increase in active chemerin. The serine proteases, elastase and tryptase were elevated in adipocyte media following treatment with TNFα and their targeted neutralization recapitulated the aprotinin-mediated effects. In contrast, bestatin, an aminopeptidase inhibitor, further elevated the TNFα-associated increase in active chemerin. Our results support that adipocytes regulate chemerin by serine protease-mediated activation pathways and aminopeptidase deactivation pathways. Following TNFα treatment, increased elastase and tryptase modify the balance between activation and deactivation, elevating active chemerin concentration in adipocyte media and subsequent CMKLR1 activation.

Indexed as

3T3-L1 CellsAdipocytesAnimalsChemokinesChemotactic FactorsCulture MediaFibrinolysisIntercellular Signaling Peptides and ProteinsLeucineLymphocytesMiceMice, Inbred C57BLModels, BiologicalPancreatic ElastaseProtease InhibitorsProteolysischemerin protein, mouseChemokinesChemotactic FactorsCMKLR1 protein, mouseCulture MediaIntercellular Signaling Peptides and ProteinsLeucinePancreatic ElastaseProtease InhibitorsReceptors, ChemokineReceptors, G-Protein-CoupledTryptasesTumor Necrosis Factor-alphaubenimex

Identifiers

PMID23227233
PMCPMC3515524
OpenAlexW2073034432

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.