The effect of different molecular weight hyaluronan on macrophage physiology
Language English Country Sweden Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
20027154
PII: NEL300709A17
Knihovny.cz E-resources
- MeSH
- Macrophage Activation drug effects physiology MeSH
- Hyaluronan Receptors metabolism MeSH
- Cell Line MeSH
- Hyaluronic Acid chemistry metabolism pharmacology MeSH
- Lipopolysaccharides toxicity MeSH
- Macrophages chemistry drug effects physiology MeSH
- Molecular Weight MeSH
- Mice MeSH
- NF-kappa B metabolism MeSH
- Nitric Oxide metabolism MeSH
- Flow Cytometry MeSH
- Nitric Oxide Synthase Type II metabolism MeSH
- Tumor Necrosis Factor-alpha metabolism MeSH
- Toll-Like Receptor 2 metabolism MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Hyaluronan Receptors MeSH
- Cd44 protein, mouse MeSH Browser
- Hyaluronic Acid MeSH
- Lipopolysaccharides MeSH
- NF-kappa B MeSH
- Nos2 protein, mouse MeSH Browser
- Nitric Oxide MeSH
- Nitric Oxide Synthase Type II MeSH
- Tlr2 protein, mouse MeSH Browser
- Tumor Necrosis Factor-alpha MeSH
- Toll-Like Receptor 2 MeSH
OBJECTIVES: Hyaluronan, a linear glycosaminoglycan, is an abundant component of extracellular matrix. In its native form, the high-molar-mass hyaluronan polymers have an array of structural and regulatory, mainly anti-inflammatory and anti-angiogenic, functions. In contradiction, the biological effects of fragmented low molecular weight hyaluronan are suggested to be pro-angiogenic and pro-inflammatory. METHODS: The effects of highly purified pharmacological grade hyaluronan of defined molecular weights 11, 52, 87, 250 and 970 kilodaltons were tested on mouse macrophage cell lines RAW 264.7 and MHS. The surface expression of CD44 and Toll-like receptor 2, surface receptors for hyaluronan, was determined by flow cytometry. Activation of macrophages was determined based on nitric oxide and tumour necrosis factor alpha production, inducible nitric oxide synthase expression, and the activation of the nuclear factor kappa B transcriptional factor. RESULTS: Both macrophage cell lines expressed CD44 and Toll-like receptor 2, which were significantly increased by the pre-treatment of macrophages with bacterial lipopolysaccharide. Hyaluronan of any molecular weight did not activate production of nitric oxide or tumour necrosis factor alpha in any mouse macrophage cell lines. Correspondingly, hyaluronan of any tested molecular weight did not stimulate nuclear factor kappa B activation. Similarly, hyaluronan of any molecular weight neither exerted stimulatory nor inhibitory effects on macrophages pre-treated by lipopolysaccharide. CONCLUSION: Interestingly, the data does not support the current view of low molecular weight hyaluronan as a pro-inflammatory mediator for macrophages. Further studies are necessary to clarify the effects of different molecular weight hyaluronan on phagocytes.
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The potency of hyaluronan of different molecular weights in the stimulation of blood phagocytes
