Evidence map›Paper›PMID 29141676›Full record

ArticleArthritis research & therapy2017

Platelets are activated in ANCA-associated vasculitis via thrombin-PARs pathway and can activate the alternative complement pathway.

Di Miao, Dan-Yang Li, Min Chen, Ming-Hui Zhao

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.5field-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

30 citing papers in PubMed, 52 citations in OpenAlex.

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  16. The complement system and autoimmune diseases.Chronic diseases and translational medicine · 2022
    Review
  17. Immature Platelet Fraction and Thrombin Generation: Preeclampsia Biomarkers.Revista brasileira de ginecologia e obstetricia : revista da Federacao Brasileira das Sociedades de Ginecologia e Obstetricia · 2022
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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

4 authors at 3 institutions in 2 countries.

Di MiaoRenal Division, Department of Medicine, Peking University First Hospital, Beijing, 100034, China.
Dan-Yang LiRenal Division, Department of Medicine, Peking University First Hospital, Beijing, 100034, China.
Min ChenRenal Division, Department of Medicine, Peking University First Hospital, Beijing, 100034, China. chenmin74@sina.com.
Ming-Hui ZhaoRenal Division, Department of Medicine, Peking University First Hospital, Beijing, 100034, China.
Peking University First Hospital · CNCenter for Life Sciences · CNMinistry of Education · RO

Funding

Chinese National Natural Science Fund 81370829Chinese National Natural Science Fund 81425008Chinese National Natural Science Fund 81621092the grant from National Key Research and Development Program 2016YFC0906102
6 · The paper itself

Abstract

backgroundIn this study, we investigated the mechanism of platelet activation in patients with antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), as well as the activation of the alternative complement pathway by platelets in AAV.

methodsCD62P and platelet-leukocyte aggregates in AAV patients were tested by flow cytometry. Platelets were stimulated by plasma from active AAV patients. The effect of the thrombin-protease-activated receptors (PARs) pathway was evaluated by blocking thrombin or PAR1 antagonists. After platelets were activated by plasma from AAV patients, Ca/Mg-Tyrode's buffer and Mg-EGTA buffer were used to measure complement activation in liquid phase and on the surface of platelets.

resultsThe levels of CD62P-expressing platelets and platelet-leukocyte aggregates were significantly higher in active AAV patients than those in remission and normal controls. Platelets were activated by plasma from active AAV patients (percentage of CD62P-expressing platelets, 97.7 ± 3% vs. 1 ± 0.2%, p < 0.0001, compared with those incubated with healthy donor plasma), and this was inhibited by thrombin or PAR1 antagonists (percentage of CD62P-expressing platelets, 97.7 ± 3% vs. 2.7 ± 1%, p < 0.0001, 97.7 ± 3% vs. 5 ± 1.4%, p < 0.0001, respectively). Platelets activated by plasma from AAV patients could trigger complement activation via the alternative pathway, as demonstrated by significant elevation of C3a, C5a, and sC5b-9 and significantly more C3c and C5b-9 deposition on the surface of platelets.

conclusionsPlatelets were activated in AAV patients, and such activation was at least partially attributed to the thrombin-PARs pathway. Activated platelets triggered the alternative complement pathway in AAV.

Indexed as

AgedAnti-Neutrophil Cytoplasmic Antibody-Associated VasculitisBlood PlateletsComplement Pathway, AlternativeComplement System ProteinsFemaleHumansMaleMiddle AgedPlatelet ActivationPlatelet Aggregation InhibitorsP-SelectinReceptor, PAR-1Signal TransductionThrombinComplement System ProteinsPlatelet Aggregation InhibitorsP-SelectinReceptor, PAR-1ThrombinANCAComplementPlateletsProtease-activated receptorsThrombinVasculitis

Identifiers

PMID29141676
PMCPMC5688714
OpenAlexW2770552294

What OpenQuestion holds

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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.