Evidence map›Paper›PMID 22505518›Full record

ArticleBiological chemistry2012

Kallikrein 6 is a novel molecular trigger of reactive astrogliosis.

Isobel A Scarisbrick, Maja Radulovic, Joshua E Burda, Nadya Larson, Sachiko I Blaber, Caterina Giannini, Michael Blaber, Alexander G Vandell

Abstract read
In one paragraph

Article in Biological chemistry, 2012. 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
2.6field-weighted citation impact, top 11% 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, 52 citations in OpenAlex.

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  9. Blocking the Thrombin Receptor Promotes Repair of Demyelinated Lesions in the Adult Brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 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

8 authors at 2 institutions in 1 country.

Isobel A ScarisbrickNeurobiology of Disease Program, Mayo Medical and Graduate School, Rochester, MN 55905, USA. Scarisbrick.Isobel@mayo.edu
Maja Radulovic
Joshua E Burda
Nadya Larson
Sachiko I Blaber
Caterina Giannini
Michael Blaber
Alexander G Vandell
Mayo Clinic in Arizona · USFlorida State University · US

Funding

Targeted MV-CEA as a Potent Antitumor Agent against GBMP50CA108961 · NCI · MAYO CLINIC ROCHESTER · PI O'NEILL, BRIAN PATRICK · 2004 to 2015
$22.5M
Role of Protease Activated Receptors in Spinal Cord Injury and RepairR01NS052741 · NINDS · MAYO CLINIC ROCHESTER · PI SCARISBRICK, ISOBEL A · 2008 to 2017
$3.6M
Interactions between CNS-specific human kallikreins and the PA system in inflammaR15NS057771 · NINDS · FLORIDA STATE UNIVERSITY · PI BLABER, MICHAEL · 2007 to 2009
$228k
NCI NIH HHS P50 CA108961NCI NIH HHS P50CA108961NINDS NIH HHS R01 NS052741NINDS NIH HHS R01NS052741NINDS NIH HHS R15 NS057771NINDS NIH HHS R15NS057771-01
6 · The paper itself

Abstract

Kallikrein-related peptidase 6 (KLK6) is a trypsin-like serine protease upregulated at sites of central nervous system (CNS) injury, including de novo expression by reactive astrocytes, yet its physiological actions are largely undefined. Taken with recent evidence that KLK6 activates G-protein-coupled protease-activated receptors (PARs), we hypothesized that injury-induced elevations in KLK6 contribute to the development of astrogliosis and that this occurs in a PAR-dependent fashion. Using primary murine astrocytes and the Neu7 astrocyte cell line, we show that KLK6 causes astrocytes to transform from an epitheliod to a stellate morphology and to secrete interleukin 6 (IL-6). By contrast, KLK6 reduced expression of glial fibrillary acidic protein (GFAP). The stellation-promoting activities of KLK6 were shown to be dependent on activation of the thrombin receptor, PAR1, as a PAR1-specific inhibitor, SCH79797, blocked KLK6-induced morphological changes. The ability of KLK6 to promote astrocyte stellation was also shown to be linked to activation of protein kinase C (PKC). These studies indicate that KLK6 is positioned to serve as a molecular trigger of select physiological processes involved in the development of astrogliosis and that this is likely to occur at least in part by activation of the G-protein-coupled receptor, PAR1.

Indexed as

AnimalsAstrocytesBrainCarrier ProteinsCell ProliferationDNA-Binding ProteinsGene Expression RegulationGlial Fibrillary Acidic ProteinGliosisHumansHypertrophyInterleukin-6KallikreinsMiceProtein Kinase CReceptor, PAR-1Carrier ProteinsDNA-Binding ProteinsGlial Fibrillary Acidic ProteinInterleukin-6KallikreinsKLK6 protein, humanPARPBP protein, humanProtein Kinase CReceptor, PAR-1

Identifiers

PMID22505518
PMCPMC3335747
OpenAlexW2091128305

What OpenQuestion holds

Textmetadata
LicenceTDM
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.