Evidence map›Paper›PMID 27566567›Full record

ArticleOncotarget2016

Natural nitration of CXCL12 reduces its signaling capacity and chemotactic activity in vitro and abrogates intra-articular lymphocyte recruitment in vivo.

Rik Janssens, Anneleen Mortier, Daiane Boff, Vincent Vanheule, Mieke Gouwy, Charlotte Franck, Olav Larsen, Mette M Rosenkilde, Jo Van Damme, Flávio A Amaral and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. CXCL12/SDF-1 in IgG4-Related Disease.Frontiers in pharmacology · 2021
    Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. The unique structural and functional features of CXCL12.Cellular & molecular immunology · 2018
    Review
  14. Review
  15. Neutrophils: Beneficial and Harmful Cells in Septic Arthritis.International journal of molecular sciences · 2018
    Review
  16. Article
  17. Review
  18. Article
  19. 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

13 authors at 4 institutions in 3 countries.

Rik JanssensLaboratory of Molecular Immunology, Department of Microbiology and Immunology, Rega Institute, KU Leuven, B-3000 Leuven, Belgium.
Anneleen MortierLaboratory of Molecular Immunology, Department of Microbiology and Immunology, Rega Institute, KU Leuven, B-3000 Leuven, Belgium.
Daiane BoffLaboratory of Molecular Immunology, Department of Microbiology and Immunology, Rega Institute, KU Leuven, B-3000 Leuven, Belgium.
Vincent VanheuleLaboratory of Molecular Immunology, Department of Microbiology and Immunology, Rega Institute, KU Leuven, B-3000 Leuven, Belgium.
Mieke GouwyLaboratory of Molecular Immunology, Department of Microbiology and Immunology, Rega Institute, KU Leuven, B-3000 Leuven, Belgium.
Charlotte FranckLaboratory of Molecular Immunology, Department of Microbiology and Immunology, Rega Institute, KU Leuven, B-3000 Leuven, Belgium.
Olav LarsenLaboratory for Molecular Pharmacology, Department of Neuroscience and Pharmacology, Faculty of Health and Medical Sciences, The Panum Institute, University of Copenhagen, DK-2200 Copenhagen, Denmark.
Mette M RosenkildeLaboratory for Molecular Pharmacology, Department of Neuroscience and Pharmacology, Faculty of Health and Medical Sciences, The Panum Institute, University of Copenhagen, DK-2200 Copenhagen, Denmark.
Jo Van DammeLaboratory of Molecular Immunology, Department of Microbiology and Immunology, Rega Institute, KU Leuven, B-3000 Leuven, Belgium.
Flávio A AmaralDepartamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brasil.
Mauro M TeixeiraDepartamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brasil.
Sofie StruyfLaboratory of Molecular Immunology, Department of Microbiology and Immunology, Rega Institute, KU Leuven, B-3000 Leuven, Belgium.
Paul ProostLaboratory of Molecular Immunology, Department of Microbiology and Immunology, Rega Institute, KU Leuven, B-3000 Leuven, Belgium.
Rega Institute for Medical Research · BEUniversidade Federal de Minas Gerais · BRUniversity of Copenhagen · DKKU Leuven · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The chemokine CXCL12/stromal cell-derived factor-1 is important for leukocyte migration to lymphoid organs and inflamed tissues and stimulates tumor development. In vitro, CXCL12 activity through CXCR4 is abolished by proteolytic processing. However, limited information is available on in vivo effects of posttranslationally modified CXCL12. Natural CXCL12 was purified from the coculture supernatant of stromal cells stimulated with leukocytes and inflammatory agents. In this conditioned medium, CXCL12 with a nitration on Tyr7, designated [3-NT7]CXCL12, was discovered via Edman degradation. CXCL12 and [3-NT7]CXCL12 were chemically synthesized to evaluate the biological effects of this modification. [3-NT7]CXCL12 recruited β-arrestin 2 and phosphorylated the Akt kinase similar to CXCL12 in receptor-transfected cells. Also the affinity of CXCL12 and [3-NT7]CXCL12 for glycosaminoglycans, the G protein-coupled chemokine receptor CXCR4 and the atypical chemokine receptor ACKR3 were comparable. However, [3-NT7]CXCL12 showed a reduced ability to enhance intracellular calcium concentrations, to generate inositol triphosphate, to phosphorylate ERK1/2 and to induce monocyte and lymphocyte chemotaxis in vitro. Moreover, nitrated CXCL12 failed to induce in vivo extravasation of lymphocytes to the joint. In summary, nitration on Tyr7 under inflammatory conditions is a novel natural posttranslational regulatory mechanism of CXCL12 which may downregulate the CXCR4-mediated inflammatory and tumor-promoting activities of CXCL12.

Indexed as

Chemotaxis, LeukocyteSignal TransductionAnimalsBone Marrow CellsCalciumCell Line, TumorChemokine CXCL12ChemotaxisCHO CellsCoculture TechniquesCricetulusCulture Media, ConditionedGlycosaminoglycansHumansLymphocytesMiceCalciumChemokine CXCL12Culture Media, ConditionedCXCL12 protein, humanCxcl12 protein, mouseCXCR4 protein, humanCXCR4 protein, mouseGlycosaminoglycansReceptors, CXCR4chemokinechemotaxisextravasationlymphocyte migrationposttranslational modification

Identifiers

PMID27566567
PMCPMC5308738
OpenAlexW2513617033

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.