Evidence map›Paper›PMID 27727297›Full record

ArticlePloS one2016

Evaluating Soluble EMMPRIN as a Marker of Disease Activity in Multiple Sclerosis: Studies of Serum and Cerebrospinal Fluid.

Deepak K Kaushik, Heather Y F Yong, Jennifer N Hahn, Claudia Silva, Steven Casha, R John Hurlbert, Francois H Jacques, Robert Lisak, Omar Khan, Carolina Ionete and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.3field-weighted citation impact, top 31% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

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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

14 authors at 4 institutions in 2 countries.

Deepak K KaushikHotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada.
Heather Y F YongHotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada.
Jennifer N HahnHotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada.
Claudia SilvaHotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada.
Steven CashaHotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada.
R John HurlbertHotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada.
Francois H JacquesCSSSG-Hull Pavilion, Gatineau, Quebec, Canada.
Robert LisakMultiple Sclerosis Center, Wayne State University School of Medicine, Detroit, Michigan, United States of America.
Omar KhanMultiple Sclerosis Center, Wayne State University School of Medicine, Detroit, Michigan, United States of America.
Carolina IoneteMultiple Sclerosis Center, University of Massachusetts, Worcester, Massachusetts, United States of America.
Catherine LarochelleUniversity of Montreal, Montreal, Quebec, Canada.
Alex PratUniversity of Montreal, Montreal, Quebec, Canada.
Amit Bar-OrMontreal Neurological Institute, McGill University, Montreal, Quebec, Canada.
V Wee YongHotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada.
University of Calgary · CAUniversité de Montréal · CAWayne State University · USMontreal Neurological Institute and Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Extracellular matrix metalloproteinase inducer (EMMPRIN, CD147) is an inducer of matrix metalloproteinases and has roles in leukocyte activation and migration. We reported previously that in MS and its animal model, experimental autoimmune encephalomyelitis, cell surface-associated EMMPRIN was significantly elevated in leukocytes around inflammatory perivascular cuffs in the CNS. In this study we report that activated T-cells can secrete soluble form of EMMPRIN (sEMMPRIN) upon activation. As sEMMPRIN is also present in biological fluids, we determined whether sEMMPRIN is altered in the CSF and sera of MS subjects. Sera from individuals without neurological conditions served as controls, while CSFs collected from subjects undergoing discectomy, and without evidence of CNS pathology, were used as a comparator group. We found that serum levels of sEMMPRIN from clinically stable MS patients or other inflammatory conditions did not differ from control subjects. Paired serum and CSF samples demonstrated poor correlation of sEMMPRIN. Interestingly, sEMMPRIN levels were approximately 60% higher in CSFs compared to sera. sEMMPRIN CSF levels were significantly higher in secondary progressive compared to primary progressive subjects. Thus we conclude that measurement of sEMMPRIN in serum is not informative for disease activity in MS. The differential expression of sEMMPRIN in the CSF of primary and secondary progressive MS invites hypotheses of the still undefined roles of EMMPRIN in the CNS.

Indexed as

AdolescentAdultAgedAmyotrophic Lateral SclerosisAntibodiesBasiginBiomarkersCase-Control StudiesCD28 AntigensCentral Nervous System DiseasesEnzyme-Linked Immunosorbent AssayFemaleHumansImmunoglobulin GLeukocytes, MononuclearLymphocyte ActivationAntibodiesBasiginBiomarkersCD28 AntigensImmunoglobulin G

Identifiers

PMID27727297
PMCPMC5058493
OpenAlexW2531259928

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.