Evidence map›Paper›PMID 18988802›Full record

ArticleThe American journal of pathology2008

Genetic inversion in mast cell-deficient (Wsh) mice interrupts corin and manifests as hematopoietic and cardiac aberrancy.

Peter A Nigrovic, Daniel H D Gray, Tatiana Jones, Jenny Hallgren, Frank C Kuo, Blair Chaletzky, Michael Gurish, Diane Mathis, Christophe Benoist, David M Lee

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

111 citing papers in PubMed, 207 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Inactivation of cofilin-1 in Mcpt5-Cre-nf-Cfl1Frontiers in immunology · 2025
    Article
  5. Mast Cells in Cardiac Remodeling: Focus on the Right Ventricle.Journal of cardiovascular development and disease · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Mast Cell Involvement in Fibrosis in Chronic Graft-Versus-Host Disease.International journal of molecular sciences · 2021
    Review
  18. Article
  19. Article
  20. Article

51 more citing papers are in PubMed but not listed here.

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

10 authors at 3 institutions in 1 country.

Peter A NigrovicDivision of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA 02115, USA.
Daniel H D Gray
Tatiana Jones
Jenny Hallgren
Frank C Kuo
Blair Chaletzky
Michael Gurish
Diane Mathis
Christophe Benoist
David M Lee
Brigham and Women's Hospital · USBoston Children's Hospital · USJoslin Diabetes Center · US

Funding

Post-transcriptional regulation of inflammatory arthritisP01AI065858 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI BRENNER, MICHAEL B. · 2006 to 2010
$11.1M
C5a receptor on mast cells in inflammatory arthritisK08AR051321 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI NIGROVIC, PETER A · 2006 to 2010
$643k
Generation of antigen specific regulatory T cellsR21AI059745 · NIAID · UNIVERSITY OF ILLINOIS AT CHICAGO · PI VASU, CHENTHAMARAKSHAN · 2004 to 2005
$426k
NIAID NIH HHS P01 AI065858NIAID NIH HHS P01 AI065858-02NIAID NIH HHS R01-AI059745NIAID NIH HHS R21 AI059745NIAMS NIH HHS K08 AR051321NIAMS NIH HHS K08-AR051321
6 · The paper itself

Abstract

Mast cells participate in pathophysiological processes that range from antimicrobial defense to anaphylaxis and inflammatory arthritis. Much of the groundwork for the understanding of mast cells was established in mice that lacked mast cells through defects in either stem cell factor or its receptor, Kit. Among available strains, C57BL/6-Kit(W-sh) (W(sh)) mice are experimentally advantageous because of their background strain and fertility. However, the genetic inversion responsible for the W(sh) phenotype remains poorly defined, and its effects beyond the mast cell have been incompletely characterized. We report that W(sh) animals exhibit splenomegaly with expanded myeloid and megakaryocyte populations. Hematopoietic abnormalities extend to the bone marrow and are reflected by neutrophilia and thrombocytosis. In contrast, mast cell-deficient WBB6F1-Kit(W)/Kit(W-v) (W/W(v)) mice display mild neutropenia, but no changes in circulating platelet numbers. To help define the basis for the W(sh) phenotype, a "DNA walking" strategy was used to identify the precise location of the 3' breakpoint, which was found to reside 67.5 kb upstream of Kit. The 5' breakpoint disrupts corin, a cardiac protease responsible for the activation of atrial natriuretic peptide. Consistent with this result, transcription of full-length corin is ablated and W(sh) mice develop symptoms of cardiomegaly. Studies performed using mast cell-deficient strains must consider the capacity of associated abnormalities to either expose or compensate for the missing mast cell lineage.

Indexed as

Chromosome InversionHematopoietic SystemAnimalsHeartHeart Defects, CongenitalMaleMast CellsMiceMice, Inbred C57BLPhenotypeProto-Oncogene Proteins c-kitSerine EndopeptidasesSpleenStem CellsCorin protein, mouseProto-Oncogene Proteins c-kitSerine Endopeptidases

Identifiers

PMID18988802
PMCPMC2626381
OpenAlexW2098321105

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.