Evidence map›Paper›PMID 31262781›Full record

ArticleBlood2019

Platelet hyaluronidase-2 regulates the early stages of inflammatory disease in colitis.

Aaron C Petrey, Dana R Obery, Sean P Kessler, Ash Zawerton, Bruno Flamion, Carol A de la Motte

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. TSG6 hyaluronan matrix remodeling dampens the inflammatory response during colitis.Matrix biology : journal of the International Society for Matrix Biology · 2023
    Article
  11. Review
  12. Article
  13. Article
  14. Hyaluronidases in Human Diseases.International journal of molecular sciences · 2021
    Review
  15. Hyaluronan and Its Receptors as Regulatory Molecules of the Endothelial Interface.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2021
    Review
  16. Review
  17. Article
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

6 authors at 2 institutions in 2 countries.

Aaron C PetreyDepartment of Inflammation and Immunity, Cleveland Clinic Lerner Research Institute, Cleveland, OH; and.ORCID 0000-0002-2696-599X
Dana R OberyDepartment of Inflammation and Immunity, Cleveland Clinic Lerner Research Institute, Cleveland, OH; and.
Sean P KesslerDepartment of Inflammation and Immunity, Cleveland Clinic Lerner Research Institute, Cleveland, OH; and.
Ash ZawertonDepartment of Inflammation and Immunity, Cleveland Clinic Lerner Research Institute, Cleveland, OH; and.
Bruno FlamionMolecular Physiology Research Unit, Namur Research Institute for Life Sciences, University of Namur, Namur, Belgium.
Carol A de la MotteDepartment of Inflammation and Immunity, Cleveland Clinic Lerner Research Institute, Cleveland, OH; and.
Cleveland Clinic Lerner College of Medicine · USUniversity of Namur · BE

Funding

VERSICAN PROTEOLYSIS AND REGULATION OF VASCULAR SMOOTH MUSCLEP01HL107147 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI DWEIK, RAED A. · 2011 to 2017
$16.1M
Platelet-hyaluronan interactions as regulators of inflammation and thrombosis."K99HL135265 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI PETREY, AARON CHRISTOPHER · 2017 to 2018
$280k
NHLBI NIH HHS K99 HL135265
6 · The paper itself

Abstract

Platelets are specialized cells essential for hemostasis that also function as crucial effectors capable of mediating inflammatory and immune responses. These sentinels continually survey their environment and discriminate between homeostatic and danger signals such as modified components of the extracellular matrix. The glycosaminoglycan hyaluronan (HA) is a major extracellular matrix component that coats the vascular lumen and, under normal conditions, restricts access of inflammatory cells. In response to tissue damage, the endothelial HA matrix enhances leukocyte recruitment and regulates the early stages of the inflammatory response. We have shown that platelets can degrade HA from the surface of activated endothelial cells via the enzyme hyaluronidase-2 (HYAL2) and that HYAL2 is deficient in platelets isolated from patients with inflammatory bowel disease (IBD). Platelets are known to be involved in the pathogenesis of several chronic disease states, including IBD, but they have been largely overlooked in the context of intestinal inflammation. We therefore wanted to define the mechanism by which platelet HYAL2 regulates the inflammatory response during colitis. In this study, we provide evidence that HA catabolism is disrupted in human intestinal microvascular endothelial cells isolated from patients with IBD. Furthermore, mice deficient in HYAL2 are more susceptible to an acute model of colitis, and this increased susceptibility is abrogated by transfusion of HYAL2-competent platelets. Finally, we show that platelets, via HYAL2-dependent degradation of endothelial HA, regulate the early stages of inflammation in colitis by limiting leukocyte extravasation.

Indexed as

AnimalsBlood PlateletsCells, CulturedColitisEndothelial CellsGPI-Linked ProteinsHumansHyaluronic AcidHyaluronoglucosaminidaseInflammationInflammatory Bowel DiseasesMiceMice, KnockoutGPI-Linked ProteinsHyal2 protein, mouseHyaluronic AcidHyaluronoglucosaminidase

Identifiers

PMID31262781
PMCPMC6716076
OpenAlexW2953498371

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.