Evidence map›Paper›PMID 25837581›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2015

Role of the store-operated calcium entry protein, STIM1, in neutrophil chemotaxis and infiltration into a murine model of psoriasis-inflamed skin.

Natacha Steinckwich, Page Myers, Kyathanahalli S Janardhan, Norris D Flagler, Debra King, John G Petranka, James W Putney

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.6field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 40 citations in OpenAlex.

  1. CRAC channels as targets for immunotherapy.Current opinion in immunology · 2026
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  13. ORAI1 and ORAI2 modulate murine neutrophil calcium signaling, cellular activation, and host defense.Proceedings of the National Academy of Sciences of the United States of America · 2020
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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

7 authors at 2 institutions in 1 country.

Natacha Steinckwich*Signal Transduction Laboratory, Comparative Medicine Branch, Integrated Laboratory Systems, Incorporated, Cellular and Molecular Pathology Branch,National Toxicology Program, and Special Techniques Group, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA.
Page Myers*Signal Transduction Laboratory, Comparative Medicine Branch, Integrated Laboratory Systems, Incorporated, Cellular and Molecular Pathology Branch,National Toxicology Program, and Special Techniques Group, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA.
Kyathanahalli S Janardhan*Signal Transduction Laboratory, Comparative Medicine Branch, Integrated Laboratory Systems, Incorporated, Cellular and Molecular Pathology Branch,National Toxicology Program, and Special Techniques Group, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA.
Norris D Flagler*Signal Transduction Laboratory, Comparative Medicine Branch, Integrated Laboratory Systems, Incorporated, Cellular and Molecular Pathology Branch,National Toxicology Program, and Special Techniques Group, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA.
Debra King*Signal Transduction Laboratory, Comparative Medicine Branch, Integrated Laboratory Systems, Incorporated, Cellular and Molecular Pathology Branch,National Toxicology Program, and Special Techniques Group, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA.
John G Petranka*Signal Transduction Laboratory, Comparative Medicine Branch, Integrated Laboratory Systems, Incorporated, Cellular and Molecular Pathology Branch,National Toxicology Program, and Special Techniques Group, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA.
James W Putney*Signal Transduction Laboratory, Comparative Medicine Branch, Integrated Laboratory Systems, Incorporated, Cellular and Molecular Pathology Branch,National Toxicology Program, and Special Techniques Group, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA putney@niehs.nih.gov.
National Institute of Environmental Health Sciences · USNational Institutes of Health · US

Funding

Molecular Genetics Support to Identify Gene/Environment Interactions in DiseaseZICES102546 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI GERRISH, KEVIN · 2009 to 2025
$30.5M
Capacitative Calcium EntryZIAES090087 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BIRD, GARY · 2009 to 2019
$22.0M
Intramural NIH HHS
6 · The paper itself

Abstract

Stromal interaction molecule 1 (STIM1) is a Ca(2+) sensor protein that initiates store-operated calcium entry (SOCE). STIM1 is known to be involved in the chemoattractant signaling pathway for FPR1 in cell lines, but its role in in vivo functioning of neutrophils is unclear. Plaque-type psoriasis is a chronic inflammatory skin disorder associated with chemoattractants driving neutrophils into the epidermis. We investigated the involvement of STIM1 in neutrophil chemotaxis in vitro, as well as during chronic psoriatic inflammation. To this end, we used conditional knockout (KO) mice lacking STIM1 in cells of myeloid lineage (STIM1(fl/fl) LysM-cre). We demonstrate that STIM1 is required for chemotaxis because of multiple chemoattractants in mouse neutrophils in vitro. Using an imiquimod-induced psoriasis-like skin model, we show that KO mice had less neutrophil infiltration in the epidermis than controls, whereas neither chemoattractant production in the epidermis nor macrophage migration was decreased. KO mice displayed a more rapid reversal of the outward signs of psoriasis (plaques). Thus, KO of STIM1 impairs neutrophil contribution to psoriatic inflammation. Our data provide new insights to our understanding of how STIM1 orchestrates the cellular behavior underlying chemotaxis and illustrate the important role of SOCE in a disease-related pathologic model.

Indexed as

AminoquinolinesAnimalsCalcium ChannelsChemotaxis, LeukocyteDisease Models, AnimalHL-60 CellsHumansImiquimodIn Vitro TechniquesMembrane ProteinsMiceMice, KnockoutNeoplasm ProteinsNeutrophil InfiltrationNeutrophilsPsoriasisAminoquinolinesCalcium ChannelsImiquimodMembrane ProteinsNeoplasm ProteinsRNA, Small InterferingSTIM1 protein, humanStim1 protein, mouseStromal Interaction Molecule 1calcium signalingchronic inflammatory diseaseleukocyte migration

Identifiers

PMID25837581
PMCPMC4478797
OpenAlexW2000563705

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.