ArticleInnate immunity2018
Fragmented hyaluronan has no alarmin function assessed in arthritis synovial fibroblast and chondrocyte cultures.
Article in Innate immunity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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.
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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.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- ECM-binding properties of extracellular vesicles: advanced delivery strategies for therapeutic applications in bone and joint diseases.Cell communication and signaling : CCS · 2025Review
- Characterization of a NaWorld journal of microbiology & biotechnology · 2025Article
- A comprehensive review on microbial hyaluronan-degrading enzymes: from virulence factors to biotechnological tools.Bioresources and bioprocessing · 2024Review
- RNA Sequencing Revealed a Weak Response of Gingival Fibroblasts Exposed to Hyaluronic Acid.Bioengineering (Basel, Switzerland) · 2024Article
- Effect of Low-Molecular-Weight Hyaluronate-Based Nanoparticles on the In Vitro Expression of Cartilage Markers.International journal of molecular sciences · 2024Article
- Molecular Mechanisms in Pathophysiology of Mucopolysaccharidosis and Prospects for Innovative Therapy.International journal of molecular sciences · 2024Review
- Hyaluronic Acid in Rheumatology.Pharmaceutics · 2023Review
- Hyaluronan promotes intracellular ROS production and apoptosis in TNFα-stimulated neutrophils.Frontiers in immunology · 2023Article
- Selective isolation of hyaluronan by solid phase adsorption to silica.Analytical biochemistry · 2022Article
- Hyaluronic Acid Oligosaccharide Derivatives Alleviate Lipopolysaccharide-Induced Inflammation in ATDC5 Cells by Multiple Mechanisms.Molecules (Basel, Switzerland) · 2022Article
- Expression and activity of hyaluronidases HYAL-1, HYAL-2 and HYAL-3 in the human intervertebral disc.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2020Article
- Role of Hyaluronan in Inflammatory Effects on Human Articular Chondrocytes.Inflammation · 2019Article
- Degradation of tumour stromal hyaluronan by small extracellular vesicle-PH20 stimulates CD103Journal of extracellular vesicles · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyaluronan (HA) is a large polymer and an important component of the extracellular matrix. During homeostasis, high molecular mass HA is the predominant form, but upon inflammation, degradation products of HA accumulate. These HA fragments (HA-fs) have been reported to possess pro-inflammatory activities and thus act as alarmins, notifying immune cells of danger via TLR4 and CD44. HA is found in large quantities in synovial joint fluid. In order to reveal a potential role of HA-fs in arthritis pathogenesis, the in vitro effects of HA of various molecular masses (from 1680 kDa to oligosaccharide HA) on synovial fibroblasts and chondrocytes from rheumatoid arthritis patients, and on peripheral blood mononuclear cells from healthy donors, were investigated. TLR4 and CD44 surface expression was confirmed by immunocytochemistry, and cell activation was determined based on cytokine and chemokine production. While the cell types investigated expressed TLR4 and CD44, no increased release of IL-1ß, IL-6, IL-8, IL-10, IL-12 or TNF-α was detected after HA stimulation. Similarly, HA did not enhance activation after priming cells with low doses of LPS or by forming complexes with LPS. Hence, this study does not support the common view of HA-fs being pro-inflammatory mediators and it is not likely that HA-fs generated during arthritis contribute to disease pathogenesis.
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Registered trials
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.