Evidence map›Paper›PMID 34952603›Full record

ArticleJournal of neuroinflammation2021

Spleen tyrosine kinase facilitates neutrophil activation and worsens long-term neurologic deficits after spinal cord injury.

Dylan A McCreedy, Clare L Abram, Yongmei Hu, Sun Won Min, Madison E Platt, Megan A Kirchhoff, Shelby K Reid, Frank L Jalufka, Clifford A Lowell

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

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  13. Spinal cord injury: molecular mechanisms and therapeutic interventions.Signal transduction and targeted therapy · 2023
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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

9 authors at 2 institutions in 1 country.

Dylan A McCreedyDepartment of Biology, Texas A&M University, 301 Old Main Dr, ILSB 3128, College Station, TX, 77843, USA. dmccreedy@bio.tamu.edu.ORCID http://orcid.org/0000-0003-2413-0793
Clare L AbramDepartment of Laboratory Medicine and Immunology Program, University of California, San Francisco, CA, 94143, USA.
Yongmei HuDepartment of Laboratory Medicine and Immunology Program, University of California, San Francisco, CA, 94143, USA.
Sun Won MinDepartment of Biology, Texas A&M University, 301 Old Main Dr, ILSB 3128, College Station, TX, 77843, USA.
Madison E PlattDepartment of Biology, Texas A&M University, 301 Old Main Dr, ILSB 3128, College Station, TX, 77843, USA.
Megan A KirchhoffDepartment of Biology, Texas A&M University, 301 Old Main Dr, ILSB 3128, College Station, TX, 77843, USA.
Shelby K ReidTexas A&M Institute for Neuroscience, Texas A&M University, College Station, TX, 77843, USA.
Frank L JalufkaDepartment of Biology, Texas A&M University, 301 Old Main Dr, ILSB 3128, College Station, TX, 77843, USA.
Clifford A LowellDepartment of Laboratory Medicine and Immunology Program, University of California, San Francisco, CA, 94143, USA.
Texas A&M University · USUniversity of California, San Francisco · US

Funding

Regulation of Innate Immune Signaling by Lyn KinaseR01AI113272 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOWELL, CLIFFORD A · 2015 to 2019
$2.0M
Supplement: L-selectin shedding as a novel therapeutic strategy to mitigate acute secondary damage after spinal cord injuryR01NS122961 · NINDS · TEXAS A&M UNIVERSITY · PI MCCREEDY, DYLAN A. · 2021 to 2025
$2.0M
The role of L-selectin in leukocyte recruitment and longer term recovery after spinal cord injuryF32NS096883 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MCCREEDY, DYLAN A. · 2016 to 2018
$174k
National Institute of Allergy and Infectious Diseases RO1AI113272NIAID NIH HHS R01 AI113272NINDS NIH HHS F32 NS096883NINDS NIH HHS F32NS096883NINDS NIH HHS R01 NS122961
6 · The paper itself

Abstract

backgroundSpinal cord injury elicits widespread inflammation that can exacerbate long-term neurologic deficits. Neutrophils are the most abundant immune cell type to invade the spinal cord in the early acute phase after injury, however, their role in secondary pathogenesis and functional recovery remains unclear. We have previously shown that neutrophil functional responses during inflammation are augmented by spleen tyrosine kinase, Syk, a prominent intracellular signaling enzyme. In this study, we evaluated the contribution of Syk towards neutrophil function and long-term neurologic deficits after spinal cord injury.

methodsContusive spinal cord injury was performed at thoracic vertebra level 9 in mice with conditional deletion of Syk in neutrophils (Syk

resultsSyk deficiency in neutrophils improved long-term functional recovery after spinal cord injury, but did not promote long-term white matter sparing. Neutrophil activation, cytokine expression, and cell death in the acutely injured spinal cord were attenuated by the genetic loss of Syk while neutrophil infiltration and effector functions were not affected. Acute blood-spinal cord barrier disruption was also unaffected by Syk deficiency in neutrophils.

conclusionsSyk facilitates specific neutrophil functional responses to spinal cord injury including activation, cytokine expression, and cell death. Long-term neurologic deficits are exacerbated by Syk signaling in neutrophils independent of acute blood-spinal cord barrier disruption and long-term white matter sparing. These findings implicate Syk in pathogenic neutrophil activities that worsen long-term functional recovery after spinal cord injury.

Indexed as

Neutrophil ActivationAnimalsApoptosisCell DeathChemokinesCytokinesFemaleHindlimbMaleMiceMice, Inbred C57BLNervous System DiseasesNeutrophil InfiltrationRecovery of FunctionSpinal Cord InjuriesSpleenChemokinesCytokinesSyk KinaseSyk protein, mouseApoptosisCytokinesDegranulationInflammationNeutrophil extracellular trapsNeutrophilsSpinal cord injury

Identifiers

PMID34952603
PMCPMC8705173
OpenAlexW4200426963

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.