Evidence map›Paper›PMID 31165998›Full record

Trial reportInternational journal of hematology2019

Soluble CLEC-2 is generated independently of ADAM10 and is increased in plasma in acute coronary syndrome: comparison with soluble GPVI.

Osamu Inoue, Makoto Osada, Junya Nakamura, Fuminori Kazama, Toshiaki Shirai, Nagaharu Tsukiji, Tomoyuki Sasaki, Hiroshi Yokomichi, Tomotaka Dohi, Makoto Kaneko and 10 more

Abstract readClinical TrialComparative Study
PubMed Publisher
In one paragraph

Trial report in International journal of hematology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  4. A nonactivatingBlood vessels, thrombosis & hemostasis · 2025
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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

20 authors at 6 institutions in 1 country.

Osamu InoueInfection Control Office, University of Yamanashi Hospital, Faculty of Medicine, University of Yamanashi, Yamanashi, Japan.
Makoto OsadaDepartment of Clinical and Laboratory Medicine, Faculty of Medicine, University of Yamanashi, 1110 Shimokato, Chuo, Yamanashi, 409-3898, Japan.
Junya NakamuraDepartment of Antibody Group, Narita R&D Department, Research and Development Division, LSI Medience Corporation, Chiba, Japan.
Fuminori KazamaDepartment of Clinical and Laboratory Medicine, Faculty of Medicine, University of Yamanashi, 1110 Shimokato, Chuo, Yamanashi, 409-3898, Japan.
Toshiaki ShiraiDepartment of Clinical and Laboratory Medicine, Faculty of Medicine, University of Yamanashi, 1110 Shimokato, Chuo, Yamanashi, 409-3898, Japan.
Nagaharu TsukijiDepartment of Clinical and Laboratory Medicine, Faculty of Medicine, University of Yamanashi, 1110 Shimokato, Chuo, Yamanashi, 409-3898, Japan.
Tomoyuki SasakiDepartment of Clinical and Laboratory Medicine, Faculty of Medicine, University of Yamanashi, 1110 Shimokato, Chuo, Yamanashi, 409-3898, Japan.
Hiroshi YokomichiDepartment of Health Sciences, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Yamanashi, Japan.
Tomotaka DohiDepartment of Cardiovascular Medicine, Juntendo University School of Medicine, Tokyo, Japan.
Makoto KanekoDepartment of Laboratory Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Makoto KuranoDepartment of Laboratory Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Mitsuru OosawaDepartment of Antibody Group, Narita R&D Department, Research and Development Division, LSI Medience Corporation, Chiba, Japan.
Shogo TamuraDepartment of Clinical and Laboratory Medicine, Faculty of Medicine, University of Yamanashi, 1110 Shimokato, Chuo, Yamanashi, 409-3898, Japan.
Kaneo SatohDepartment of Clinical and Laboratory Medicine, Faculty of Medicine, University of Yamanashi, 1110 Shimokato, Chuo, Yamanashi, 409-3898, Japan.
Katsuhiro TakanoDepartment of Clinical and Laboratory Medicine, Faculty of Medicine, University of Yamanashi, 1110 Shimokato, Chuo, Yamanashi, 409-3898, Japan.
Katsumi MiyauchiDepartment of Cardiovascular Medicine, Juntendo University School of Medicine, Tokyo, Japan.
Hiroyuki DaidaDepartment of Cardiovascular Medicine, Juntendo University School of Medicine, Tokyo, Japan.
Yutaka YatomiDepartment of Laboratory Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Yukio OzakiFuefuki Chuo Hospital, Yamanashi, Japan.
Katsue Suzuki-InoueDepartment of Clinical and Laboratory Medicine, Faculty of Medicine, University of Yamanashi, 1110 Shimokato, Chuo, Yamanashi, 409-3898, Japan. katsuei@yamanashi.ac.jp.ORCID http://orcid.org/0000-0001-9678-1451
University of Yamanashi Hospital · JPJuntendo University · JPThe University of Tokyo · JPGumma Paz College · JPJapan Society for the Promotion of Science · JPUniversity of Yamanashi · JP

Funding

Japan Society for the Promotion of Science LS-052
6 · The paper itself

Abstract

Soluble forms of platelet membrane proteins are released upon platelet activation. We previously reported that soluble C-type lectin-like receptor 2 (sCLEC-2) is released as a shed fragment (Shed CLEC-2) or as a whole molecule associated with platelet microparticles (MP-CLEC-2). In contrast, soluble glycoprotein VI (sGPVI) is released as a shed fragment (Shed GPVI), but not as a microparticle-associated form (MP-GPVI). However, mechanism of sCLEC-2 generation or plasma sCLEC-2 has not been fully elucidated. Experiments using metalloproteinase inhibitors/stimulators revealed that ADAM10/17 induce GPVI shedding, but not CLEC-2 shedding, and that shed CLEC-2 was partially generated by MMP-2. Although MP-GPVI was not generated, it was generated in the presence of the ADAM10 inhibitor. Moreover, antibodies against the cytoplasmic or extracellular domain of GPVI revealed the presence of the GPVI cytoplasmic domain, but not the extracellular domain, in the microparticles. These findings suggest that most of the GPVI on microparticles are induced to shed by ADAM10; MP-GPVI is thus undetected. Plasma sCLEC-2 level was 1/32 of plasma sGPVI level in normal subjects, but both soluble proteins significantly increased in plasma of patients with acute coronary syndrome. Thus, sCLEC-2 and sGPVI are released by different mechanisms and released in vivo upon platelet activation.

Indexed as

Acute Coronary SyndromeADAM10 ProteinAmyloid Precursor Protein SecretasesCross-Sectional StudiesFemaleHumansLectins, C-TypeMaleMembrane GlycoproteinsMembrane ProteinsPlatelet Membrane GlycoproteinsProspective StudiesADAM10 ProteinADAM10 protein, humanAmyloid Precursor Protein SecretasesCLEC2B protein, humanLectins, C-TypeMembrane GlycoproteinsMembrane ProteinsPlatelet Membrane Glycoproteinsplatelet membrane glycoprotein VIADAM10BiomarkerPlateletsSoluble CLEC-2Soluble GPVI

Identifiers

PMID31165998
OpenAlexW2952263730

What OpenQuestion holds

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Registered trials

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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.