Evidence map›Paper›PMID 32949998›Full record

ArticleEBioMedicine2020

Endothelial damage and a thin intercellular fibrin network promote haemorrhage in acute promyelocytic leukaemia.

Chunxu Wang, Muxin Yu, Peng Zhou, Baorong Li, Yingmiao Liu, Lixiu Wang, Xiaojing Chen, Jingwen Du, Yufeng Wang, Jinming Zhang and 9 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EBioMedicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
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

19 authors at 3 institutions in 2 countries.

Chunxu WangDepartment of Hematology, The First Hospital, Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin 150001, China; The Key Laboratory of Myocardial Ischemia, Ministry of Education, Heilongjiang Province, Harbin, China.
Muxin YuDepartment of Hematology, The First Hospital, Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin 150001, China.
Peng ZhouThe Key Laboratory of Myocardial Ischemia, Ministry of Education, Heilongjiang Province, Harbin, China; Department of Neurosurgery, The Second Hospital, Harbin Medical University, Harbin, China.
Baorong LiDepartment of Hematology, The First Hospital, Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin 150001, China.
Yingmiao LiuDepartment of Hematology, The First Hospital, Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin 150001, China.
Lixiu WangDepartments of Cardiology, The First Hospital, Harbin Medical University, Harbin, China.
Xiaojing ChenDepartment of Hematology, The First Hospital, Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin 150001, China.
Jingwen DuDepartment of Hematology, The First Hospital, Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin 150001, China.
Yufeng WangDepartment of Hematology, The First Hospital, Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin 150001, China.
Jinming ZhangDepartment of Hematology, The First Hospital, Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin 150001, China.
Haijiao JingDepartment of Hematology, The First Hospital, Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin 150001, China.
Yiming FengDepartment of Hematology, The First Hospital, Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin 150001, China.
Yue ZhangDepartment of Hematology, The First Hospital, Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin 150001, China.
Yueyue LiDepartment of Hematology, The First Hospital, Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin 150001, China.
Zengxiang DongDepartments of Cardiology, The First Hospital, Harbin Medical University, Harbin, China.
Shaohong FangThe Key Laboratory of Myocardial Ischemia, Ministry of Education, Heilongjiang Province, Harbin, China.
Valerie A NovakovicDepartment of Research, VA Boston Healthcare System, Harvard Medical School, Boston, MA, USA.
Jin ZhouDepartment of Hematology, The First Hospital, Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin 150001, China.
Jialan ShiDepartment of Hematology, The First Hospital, Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin 150001, China; Department of Research, VA Boston Healthcare System, Harvard Medical School, Boston, MA, USA; Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 1400 VFW Parkway, West Roxbury, Boston, MA 02132, USA. Electronic address: jialan_shi@hms.harvard.edu.
Harbin Medical University · CNBrigham and Women's Hospital · USHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe role of vascular endothelium in acute promyelocytic leukaemia (APL) remains unknown. We aimed to investigate the mechanisms by which APL cells interact with endothelial cells (ECs) and to further explore how the endothelium affects bleeding as well as therapeutic interventions.

methodAPL cells and an original APL cell line, NB4 cells, were used for experiments. The effects of leukaemic cells on ECs were analyzed in vitro and in vivo. Moreover, the endothelial barrier function and procoagulant activity were detected. An APL mouse model was established for in vivo studies.

findingsAPL cells interacted with ECs via ICAM-1 and VCAM-1 receptors to disrupt endothelial integrity. This binding activated MLCK signaling, resulting in the trans-endothelial passage of protein and red blood cells (RBCs). Combined treatment with asiatic acid or anti-adhesion receptor antibody inhibited the response of ECs to APL cells, thereby preventing APL-associated haemorrhage in vitro and in vivo. Activated ECs exhibited a procoagulant phenotype after phosphatidylserine exposure. Plasma from APL patients formed a thin fibrin network between procoagulant ECs, and this intercellular fibrin decreased the passage of albumin and RBCs. Ex vivo addition of fibrinogen further enhanced this barrier function in a dose-dependent manner.

interpretationEndothelial damage induced by leukaemic cell adherence promotes haemorrhaging in APL. Stabilization of ECs, decreasing adhesion receptor expression, and increasing fibrinogen transfusion levels may be a new therapeutic avenue to alleviate this fatal bleeding complication.

fundingNational Science Foundation of China (81670128, 81873433).

Indexed as

AdultAgedAnimalsBiomarkersCapillary PermeabilityCell AdhesionCell CommunicationCell LineDisease Models, AnimalDisease SusceptibilityEndothelial CellsEndothelium, VascularFemaleFibrinFluorescent Antibody TechniqueHemorrhageBiomarkersFibrinAcute promyelocytic leukaemiaEndothelial cellsFibrinHaemorrhagePermeability

Identifiers

PMID32949998
PMCPMC7501057
OpenAlexW3087319097

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.