Evidence map›Paper›PMID 28730511›Full record

ArticleInflammation2017

Intermediate Molecular Mass Hyaluronan and CD44 Receptor Interactions Enhance Neutrophil Phagocytosis and IL-8 Production via p38- and ERK1/2-MAPK Signalling Pathways.

Cheng-Hsun Lu, Chia-Huei Lin, Ko-Jen Li, Chieh-Yu Shen, Cheng-Han Wu, Yu-Min Kuo, Ting-Syuan Lin, Chia-Li Yu, Song-Chou Hsieh

Abstract read
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In one paragraph

Article in Inflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

13 citing papers in PubMed, 25 citations in OpenAlex.

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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

9 authors at 3 institutions in 1 country.

Cheng-Hsun LuInstitute of Clinical Medicine, National Taiwan University College of Medicine, No. 7 Chung-San South Road, Taipei, 10002, Taiwan.
Chia-Huei LinDepartment of Internal Medicine, National Taiwan University Hospital, National Taiwan University College of Medicine, No. 7, Chung-San South Road, Taipei, 10002, Taiwan.
Ko-Jen LiDepartment of Internal Medicine, National Taiwan University Hospital, National Taiwan University College of Medicine, No. 7, Chung-San South Road, Taipei, 10002, Taiwan.
Chieh-Yu ShenInstitute of Clinical Medicine, National Taiwan University College of Medicine, No. 7 Chung-San South Road, Taipei, 10002, Taiwan.
Cheng-Han WuInstitute of Clinical Medicine, National Taiwan University College of Medicine, No. 7 Chung-San South Road, Taipei, 10002, Taiwan.
Yu-Min KuoInstitute of Clinical Medicine, National Taiwan University College of Medicine, No. 7 Chung-San South Road, Taipei, 10002, Taiwan.
Ting-Syuan LinDepartment of Internal Medicine, National Taiwan University Hospital-Yunlin Branch, No. 95 Xuefu Rd, Huwei Township, Yunlin County, 632, Taiwan.
Chia-Li YuDepartment of Internal Medicine, National Taiwan University Hospital, National Taiwan University College of Medicine, No. 7, Chung-San South Road, Taipei, 10002, Taiwan.
Song-Chou HsiehDepartment of Internal Medicine, National Taiwan University Hospital, National Taiwan University College of Medicine, No. 7, Chung-San South Road, Taipei, 10002, Taiwan. hsiehsc@ntu.edu.tw.
National Taiwan University Hospital · TWNational Taiwan University · TWNational Yunlin University of Science and Technology · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD44 is a common leukocyte adhesion molecule expressed on the surface of various cells. Hyaluronan (HA), the natural ligand of CD44, is a simple repeated disaccharide with variable molecular mass that is widely distributed on cell surfaces and the connective tissue matrix. The binding of small molecular mass HA (SMM-HA, MW < 80 kDa) to CD44 on immune-related cells elicits cell proliferation, differentiation, and cytokine production. However, the effects and molecular basis of intermediate molecular mass HA (IMM-HA, MW ≈ 500 kDa)-CD44 interactions on polymorphonuclear neutrophil (PMN) functions have not been elucidated. We hypothesised that IMM-HA would potentiate immune functions as well as SMM-HA. In the present study, we demonstrated IMM-HA and CD44 interactions enhanced normal PMN phagocytosis and IL-8 production compared to those with LPS or anti-CD45 treatment via F-actin cytoskeleton polymerization and subsequent ERK1/2- and p38-MAPK phosphorylation. Antibody-based inhibition of CD44 did not affect PMN function; however, F-actin aggregation was induced without MAPK phosphorylation. Enhanced PMN function via IMM-HA was determined to be CD44-dependent since this effect was abolished in DMSO-induced CD44(-) PMN-like cells obtained from HL-60 cells. In conclusion, we demonstrated that IMM-HA and CD44 interactions on PMNs potently elicit F-actin cytoskeleton polymerization and p38- and ERK1/2-MAPK phosphorylation to enhance PMN function.

Indexed as

PhagocytosisActinsCytoskeletonHL-60 CellsHumansHyaluronan ReceptorsHyaluronic AcidInterleukin-8MAP Kinase Signaling SystemNeutrophilsp38 Mitogen-Activated Protein KinasesPhosphorylationProtein BindingSignal TransductionActinsCD44 protein, humanHyaluronan ReceptorsHyaluronic AcidInterleukin-8p38 Mitogen-Activated Protein Kinasesantibody-induced receptor commitmentcommon leukocyte antigenF-actin cytoskeleton polymerizationglycosaminoglycan

Identifiers

PMID28730511
OpenAlexW2738430471

What OpenQuestion holds

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Registered trials

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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.