Evidence map›Paper›PMID 24128681›Full record

ArticleJournal of neuropathology and experimental neurology2013

Kallikrein cascades in traumatic spinal cord injury: in vitro evidence for roles in axonopathy and neuron degeneration.

Maja Radulovic, Hyesook Yoon, Nadya Larson, Jianmin Wu, Rachel Linbo, Joshua E Burda, Eleftherios P Diamandis, Sachiko I Blaber, Michael Blaber, Michael G Fehlings and 1 more

Open access · greenAbstract read
In one paragraph

Article in Journal of neuropathology and experimental neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 40 citations in OpenAlex.

  1. Regional Molecular Diversity in Chronic Spinal Cord Injury.Cellular and molecular neurobiology · 2026
    Article
  2. Drug Discovery Strategies for Kallikrein-Related Peptidases.International journal of molecular sciences · 2025
    Review
  3. GOBeacon: An ensemble model for protein function prediction enhanced by contrastive learning.Protein science : a publication of the Protein Society · 2025
    Article
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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

11 authors at 4 institutions in 2 countries.

Maja RadulovicFrom the Neurobiology of Disease Program (MR, JEB, IAS) and Departments of Physical Medicine and Rehabilitation (HY, NL, JW, RL, IAS) and Neurology (IAS), Mayo Medical and Graduate School, Rochester, Minnesota; Department of Pathology and Laboratory Medicine, Mount Sinai Hospital, Toronto, Ontario, Canada (EPD); Department of Biomedical Sciences, Florida State University College of Medicine, Tallahassee, Florida (SIB, MB); and Department of Surgery, Toronto Western Research Institute, Toronto, Ontario, Canada (MGF).
Hyesook Yoon
Nadya Larson
Jianmin Wu
Rachel Linbo
Joshua E Burda
Eleftherios P Diamandis
Sachiko I Blaber
Michael Blaber
Michael G Fehlings
Isobel A Scarisbrick
Mayo Clinic in Arizona · USFlorida State University · USMount Sinai Hospital · CAToronto Western Hospital · CA

Funding

Women's Cancer ProgramP30CA015083 · NCI · MAYO CLINIC ROCHESTER · PI AKHILESH PANDEY · 1985 to 2026
$151.3M
Role of Protease Activated Receptors in Spinal Cord Injury and RepairR01NS052741 · NINDS · MAYO CLINIC ROCHESTER · PI SCARISBRICK, ISOBEL A · 2008 to 2017
$3.6M
NCI NIH HHS CA1060A11NCI NIH HHS P30 CA015083NINDS NIH HHS R01 NS052741NINDS NIH HHS R01NS052741
6 · The paper itself

Abstract

Kallikreins (KLKs) are a family of 15 secreted serine proteases with emerging roles in neurologic diseases. To illuminate their contributions to the pathophysiology of spinal cord injury (SCI), we evaluated acute through chronic changes in the immunohistochemical appearance of 6 KLKs (KLK1, KLK5, KLK6, KLK7, KLK8, and KLK9) in postmortem human traumatic SCI cases, quantified their RNA expression levels in experimental murine SCI, and assessed the impact of recombinant forms of each enzyme toward murine cortical neurons in vitro. Temporally and spatially distinct changes in KLK expression were observed with partially overlapping patterns between human and murine SCI, including peak elevations (or reductions) during the acute and subacute periods. Kallikrein 9 showed the most marked changes and remained chronically elevated. Importantly, a subset of KLKs (KLK1, KLK5, KLK6, KLK7, and KLK9) were neurotoxic toward primary neurons in vitro. Kallikrein immunoreactivity was also observed in association with swollen axons and retraction bulbs in the human SCI cases examined. Together, these findings demonstrate that elevated levels of a significant subset of KLKs are positioned to contribute to neurodegenerative changes in cases of CNS trauma and disease and, therefore, represent new potential targets for the development of neuroprotective strategies.

Indexed as

AdolescentAdultAgedAnimalsAxonsChildChild, PreschoolFemaleHumansKallikreinsMaleMiceMiddle AgedNerve DegenerationSignal TransductionSpinal CordKallikreins

Identifiers

PMID24128681
PMCPMC4097185
OpenAlexW2042729398

What OpenQuestion holds

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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.