Evidence map›Paper›PMID 37494581›Full record

ArticleMicrocirculation (New York, N.Y. : 1994)2023

Removal of the endothelial surface layer via hyaluronidase does not modulate monocyte and neutrophil interactions with the glomerular endothelium.

ZheHao Tan, Pam Hall, Adam Costin, Simon A Crawford, Georg Ramm, Connie H Y Wong, A Richard Kitching, Michael J Hickey

Open access · hybridAbstract read
In one paragraph

Article in Microcirculation (New York, N.Y. : 1994), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.5field-weighted citation impact, top 31% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

8 authors at 2 institutions in 1 country.

ZheHao TanCentre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia.ORCID 0009-0009-3116-0203
Pam HallCentre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia.
Adam CostinMonash Ramaciotti Centre for Cryo-Electron Microscopy, Monash University, Clayton, Victoria, Australia.
Simon A CrawfordMonash Ramaciotti Centre for Cryo-Electron Microscopy, Monash University, Clayton, Victoria, Australia.
Georg RammMonash Ramaciotti Centre for Cryo-Electron Microscopy, Monash University, Clayton, Victoria, Australia.
Connie H Y WongCentre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia.ORCID 0000-0002-9020-1847
A Richard KitchingCentre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia.
Michael J HickeyCentre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia.ORCID 0000-0003-2354-357X
Monash Medical Centre · AUMonash University · AU

Funding

National Health and Medical Research Council 1042775National Health and Medical Research Council 1064112National Health and Medical Research Council 1124459
6 · The paper itself

Abstract

objectiveThe endothelial surface layer (ESL), a layer of macromolecules on the surface of endothelial cells, can both impede and facilitate leukocyte recruitment. However, its role in monocyte and neutrophil recruitment in glomerular capillaries is unknown.

methodsWe used multiphoton intravital microscopy to examine monocyte and neutrophil behavior in the glomerulus following ESL disruption with hyaluronidase.

resultsConstitutive retention and migration of monocytes and neutrophils within the glomerular microvasculature was unaltered by hyaluronidase. Consistent with this, inhibition of the hyaluronan-binding molecule CD44 also failed to modulate glomerular trafficking of these immune cells. To investigate the contribution of the ESL during acute inflammation, we induced glomerulonephritis via in situ immune complex deposition. This resulted in increases in glomerular retention of monocytes and neutrophils but did not induce marked reduction in the glomerular ESL. Furthermore, hyaluronidase treatment did not modify the prolonged retention of monocytes and neutrophils in the acutely inflamed glomerular microvasculature.

conclusionsThese observations indicate that, despite evidence that the ESL has the capacity to inhibit leukocyte-endothelial cell interactions while also containing adhesive ligands for immune cells, neither of these functions modulate trafficking of monocytes and neutrophils in steady-state or acutely-inflamed glomeruli.

Indexed as

MonocytesNeutrophilsEndothelial CellsEndotheliumHyaluronoglucosaminidaseHyaluronoglucosaminidaseendotheliumglomerulonephritisglomerulushyaluronaninflammation

Identifiers

PMID37494581
PMCPMC10909409
OpenAlexW4385289158

What OpenQuestion holds

Textmetadata
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.