High molecular weight hyaluronic acid inhibits advanced glycation endproduct-induced NF-κB activation and cytokine expression

Advanced glycation endproducts (AGEs), which accumulate on long-lived proteins and protein deposits (amyloids), induce the expression of proinflammatory cytokines through NF-κB-dependent pathways. Hyaluronic acid with a molecular weight above 1.2 MDa (HMW-HA) inhibits the AGE-induced activation of t...

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Bibliographic Details
Published in:FEBS letters 1999-06, Vol.453 (3), p.283-287
Main Authors: Neumann, Arne, Schinzel, Reinhard, Palm, Dieter, Riederer, Peter, Münch, Gerald
Format: Article
Language:English
Subjects:
Advanced glycation endproduct
AGE, advanced glycation endproduct
HA, hyaluronic acid
HMW, high molecular weight
Hyaluronic acid
IL-1α, interleukin 1α
IL-6, interleukin 6
LMW, low molecular weight
Signal transduction
TNF, tumor necrosis factor
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Summary:Advanced glycation endproducts (AGEs), which accumulate on long-lived proteins and protein deposits (amyloids), induce the expression of proinflammatory cytokines through NF-κB-dependent pathways. Hyaluronic acid with a molecular weight above 1.2 MDa (HMW-HA) inhibits the AGE-induced activation of the transcription factor NF-κB and the NF-κB-regulated cytokines interleukin-1α, interleukin-6 and tumor necrosis factor-α. Since the molecular weight of hyaluronic acid in humans decreases with age and under conditions of oxidative stress, it is likely that the protective effect of HMW-HA against AGE-induced cellular activation is lost at sites of chronic inflammation and in older age.
ISSN:0014-5793
1873-3468
DOI:10.1016/S0014-5793(99)00731-0