Evidence map›Paper›PMID 32929010›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2020

Hemostasis vs. homeostasis: Platelets are essential for preserving vascular barrier function in the absence of injury or inflammation.

Shuchi Gupta, Christoph Konradt, Adam Corken, Jerry Ware, Bernhard Nieswandt, Jorge Di Paola, Mei Yu, Demin Wang, Marvin T Nieman, Sidney W Whiteheart and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.3field-weighted citation impact, top 4% 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

34 citing papers in PubMed, 89 citations in OpenAlex.

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  6. Platelet effector functions in inflammation.Research and practice in thrombosis and haemostasis · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 8 institutions in 2 countries.

Shuchi GuptaDepartment of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104.ORCID 0000-0002-3634-5612
Christoph KonradtDepartment of Comparative Pathobiology, Purdue University College of Veterinary Medicine, West Lafayette, IN 47907.ORCID 0000-0003-4408-6769
Adam CorkenDepartment of Physiology and Biophysics, University of Arkansas for Medical Sciences, Little Rock, AR 72205.ORCID 0000-0002-4700-9091
Jerry WareDepartment of Physiology and Biophysics, University of Arkansas for Medical Sciences, Little Rock, AR 72205.ORCID 0000-0001-8860-6338
Bernhard NieswandtInstitute of Experimental Biomedicine, University Hospital Wuerzburg, 97080 Wuerzburg, Germany.
Jorge Di PaolaDepartment of Pediatrics, Washington University School of Medicine in St. Louis, St. Louis, MO 63110.ORCID 0000-0002-1461-2871
Mei YuHematopoiesis and B cell biology lab, Blood Research Institute, Versiti, Milwaukee, WI 53226.
Demin WangHematopoiesis and B cell biology lab, Blood Research Institute, Versiti, Milwaukee, WI 53226.
Marvin T NiemanDepartment of Pharmacology, Case Western Reserve University, Cleveland, OH 44106.ORCID 0000-0003-2602-023X
Sidney W WhiteheartDepartment of Molecular and Cellular Biochemistry, University of Kentucky, Lexington, KY 40536.ORCID 0000-0001-5577-0473
Lawrence F BrassDepartment of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104; brass@pennmedicine.upenn.edu.
Translational Therapeutics (United States) · USUniversity of Arkansas for Medical Sciences · USVersiti Blood Center of Wisconsin · USCase Western Reserve University · USPurdue University West Lafayette · USUniversity of Kentucky · USUniversity of Würzburg · DEWashington University in St. Louis · US

Funding

Subcellular Mechanisms pf Platelet ActivationP01HL040387 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI PONCZ, MORTIMER · 1988 to 2018
$35.5M
Thrombosis Models CoreP01HL120846 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI ABRAMS, CHARLES S. · 2014 to 2018
$12.2M
Studies of Physiologic and Pathologic Platelet Plug FormationP01HL146373 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI BRASS, LAWRENCE F · 2020 to 2024
$12.2M
B cell responses in heparin-induced thrombocytopeniaR01HL130724 · NHLBI · VERSITI WISCONSIN, INC. · PI WANG, DEMIN · 2017 to 2024
$4.8M
The role of protease activated receptors on platelets.R01HL098217 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI NIEMAN, MARVIN THOMAS · 2010 to 2024
$4.6M
PLC?s in B cell biology and autoimmunityR01AI079087 · NIAID · VERSITI WISCONSIN, INC. · PI WANG, DEMIN · 2008 to 2018
$4.4M
Building Enhanced Capability for the PennVet Multiphoton CoreS10OD021633 · OD · UNIVERSITY OF PENNSYLVANIA · PI FREEDMAN, BRUCE D · 2016 to 2016
$600k
NHLBI NIH HHS P01 HL040387NHLBI NIH HHS P01 HL120846NHLBI NIH HHS P01 HL146373NHLBI NIH HHS R01 HL098217NHLBI NIH HHS R01 HL130724NIAID NIH HHS R01 AI079087NIH HHS S10 OD021633
6 · The paper itself

Abstract

Platelets are best known for their vasoprotective responses to injury and inflammation. Here, we have asked whether they also support vascular integrity when neither injury nor inflammation is present. Changes in vascular barrier function in dermal and meningeal vessels were measured in real time in mouse models using the differential extravasation of fluorescent tracers as a biomarker. Severe thrombocytopenia produced by two distinct methods caused increased extravasation of 40-kDa dextran from capillaries and postcapillary venules but had no effect on extravasation of 70-kDa dextran or albumin. This reduction in barrier function required more than 4 h to emerge after thrombocytopenia was established, reverting to normal as the platelet count recovered. Barrier dysfunction was also observed in mice that lacked platelet-dense granules, dense granule secretion machinery, glycoprotein (GP) VI, or the GPVI signaling effector phospholipase C (PLC) γ2. It did not occur in mice lacking α-granules, C type lectin receptor-2 (CLEC-2), or protease activated receptor 4 (PAR4). Notably, although both meningeal and dermal vessels were affected, intracerebral vessels, which are known for their tighter junctions between endothelial cells, were not. Collectively, these observations 1) highlight a role for platelets in maintaining vascular homeostasis in the absence of injury or inflammation, 2) provide a sensitive biomarker for detecting changes in platelet-dependent barrier function, 3) identify which platelet processes are required, and 4) suggest that the absence of competent platelets causes changes in the vessel wall itself, accounting for the time required for dysfunction to emerge.

Indexed as

HemostasisHomeostasisAnimalsBlood PlateletsBlood VesselsFemaleLectins, C-TypeMaleMeningesMicePhospholipase C gammaSkinLectins, C-TypePhospholipase C gammadense granulesGPVI signalinghomeostasisplateletsvascular integrity

Identifiers

PMID32929010
PMCPMC7533880
OpenAlexW3084443989

What OpenQuestion holds

Textmetadata
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.