Evidence map›Paper›PMID 23532733›Full record

ArticleBlood2013

SerpinB1 is critical for neutrophil survival through cell-autonomous inhibition of cathepsin G.

Mathias Baumann, Christine T N Pham, Charaf Benarafa

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.0field-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

35 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Endothelial Cell Secretome Alterations Induced by Inflammatory Stress.bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. It's a Trap!-Potential of Cathepsins in NET Formation.International journal of molecular sciences · 2025
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Substituted 4H-3,1-benzoxazine-4-one Derivatives as Inhibitors of Cathepsin G.Medicinal chemistry (Shariqah (United Arab Emirates)) · 2024
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. 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

3 authors at 3 institutions in 3 countries.

Mathias BaumannTheodor Kocher Institute, University of Bern, Bern, Switzerland.
Christine T N Pham
Charaf Benarafa
Robert Koch Institute · DEUniversity of Bern · CHWashington University in St. Louis · US

Funding

ROLE OF DPPI & SERINE PROTEASES IN INFLAMMATORY DISEASESR01AI049261 · NIAID · WASHINGTON UNIVERSITY · PI PHAM, CHRISTINE T. · 2002 to 2012
$3.1M
TARGETED NANOTHERAPY IN THE TREATMENT OF INFLAMMATORY ARTHRITISR01AR056468 · NIAMS · WASHINGTON UNIVERSITY · PI PHAM, CHRISTINE T. · 2008 to 2012
$1.6M
Role of DPPI & Serine Proteases in Inflammatory DiseasesR56AI049261 · NIAID · WASHINGTON UNIVERSITY · PI PHAM, CHRISTINE T · 2007 to 2007
$342k
NIAID NIH HHS AI049261NIAID NIH HHS R01 AI049261NIAID NIH HHS R56 AI049261NIAMS NIH HHS R01 AR056468
6 · The paper itself

Abstract

Bone marrow (BM) holds a large reserve of polymorphonuclear neutrophils (PMNs) that are rapidly mobilized to the circulation and tissues in response to danger signals. SerpinB1 is a potent inhibitor of neutrophil serine proteases neutrophil elastase (NE) and cathepsin G (CG). SerpinB1 deficiency (sB1(-/-)) results in a severe reduction of the BM PMN reserve and failure to clear bacterial infection. Using BM chimera, we found that serpinB1 deficiency in BM cells was necessary and sufficient to reproduce the BM neutropenia of sB1(-/-) mice. Moreover, we showed that genetic deletion of CG, but not NE, fully rescued the BM neutropenia in sB1(-/-) mice. In mixed BM chimera and in vitro survival studies, we showed that CG modulates sB1(-/-) PMN survival through a cell-intrinsic pathway. In addition, membrane permeabilization by lysosomotropic agent l-leucyl-l-leucine methyl ester that allows cytosolic release of granule contents was sufficient to induce rapid PMN death through a CG-dependent pathway. CG-mediated PMN cytotoxicity was only partly blocked by caspase inhibition, suggesting that CG cleaves a distinct set of targets during apoptosis. In conclusion, we have unveiled a new cytotoxic function for the serine protease CG and showed that serpinB1 is critical for maintaining PMN survival by antagonizing intracellular CG activity.

Indexed as

AnimalsCathepsin GCells, CulturedCell SurvivalDown-RegulationFemaleMaleMiceMice, Inbred C57BLMice, KnockoutNeutrophilsOrgan SpecificitySerpinsCathepsin GSerpinb1a protein, mouseSerpins

Identifiers

PMID23532733
PMCPMC3650706
OpenAlexW1997002066

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.