Free radical depolymerization of hyaluronan by maillard reaction products

Deguine, V.; Ménasche, Maurice; Ferrari, Patrícia; Fraisse, Laurent; Pouliquen, Y.; Robert, L.

doi:10.1016/s0141-8130(97)00084-6

Cited by 76 publications

(61 citation statements)

References 34 publications

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“…Hyaluronidases are the main enzymes responsible for enzymatic degradation of hyaluronan, and zymography is one of the most sensitive methods to detect hyaluronidase activity. Hyaluronan can also be degraded into smaller fragments in a nonenzymatic way by exposure to reactive oxygen intermediates (72), which is believed to be an important mechanism for generating HA fragments at sites of inflammation (73). Our study shows that hyaluronidase activity did not change due to asbestos and TiO 2 treatment, which further supports the previous reports that ROS is an important mechanism for generating hyaluronan fragments at sites of inflammation.…”

Section: Discussionsupporting

confidence: 90%

Extracellular Superoxide Dismutase Inhibits Inflammation by Preventing Oxidative Fragmentation of Hyaluronan

Gao

Koenitzer

Tobolewski

et al. 2008

Journal of Biological Chemistry

162

133

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Extracellular superoxide dismutase (EC-SOD) is expressed at high levels in lungs. EC-SOD has a polycationic matrix-binding domain that binds to polyanionic constituents in the matrix. Previous studies indicate that EC-SOD protects the lung in both bleomycin-and asbestos-induced models of pulmonary fibrosis. Although the mechanism of EC-SOD protection is not fully understood, these studies indicate that EC-SOD plays an important role in regulating inflammatory responses to pulmonary injury. Hyaluronan is a polyanionic high molecular mass polysaccharide found in the extracellular matrix that is sensitive to oxidant-mediated fragmentation. Recent studies found that elevated levels of low molecular mass hyaluronan are associated with inflammatory conditions. We hypothesize that EC-SOD may inhibit pulmonary inflammation in part by preventing superoxide-mediated fragmentation of hyaluronan to low molecular mass fragments. We found that EC-SOD directly binds to hyaluronan and significantly inhibits oxidant-induced degradation of this glycosaminoglycan. In vitro human polymorphic neutrophil chemotaxis studies indicate that oxidative fragmentation of hyaluronan results in polymorphic neutrophil chemotaxis and that EC-SOD can completely prevent this response. Intratracheal injection of crocidolite asbestos in mice leads to pulmonary inflammation and injury that is enhanced in EC-SOD knock-out mice. Notably, hyaluronan levels are increased in the bronchoalveolar lavage fluid after asbestos-induced pulmonary injury, and this response is markedly enhanced in EC-SOD knock-out mice. These data indicate that inhibition of oxidative hyaluronan fragmentation probably represents one mechanism by which EC-SOD inhibits inflammation in response to lung injury.

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Section: Discussionsupporting

confidence: 90%

Extracellular Superoxide Dismutase Inhibits Inflammation by Preventing Oxidative Fragmentation of Hyaluronan

Gao

Koenitzer

Tobolewski

et al. 2008

Journal of Biological Chemistry

162

133

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“…Cell death was of a necrotic type, by lesion of the cell membrane. This observation suggested a possible role for ROS-generation by GPs, demonstrated by several authors [16,17] and studied in our laboratory also as will be described later. Table 4 shows the acceleration by GPs of the entrance of cells in the senescent state.…”

Section: Function Referencesupporting

confidence: 76%

Role of the Maillard reaction in aging and age-related diseases. Studies at the cellular-molecular level

Robert

Labat‐Robert

2014

Clinical Chemistry and Laboratory Medicine

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Increase in life expectancy concerns most populations but more importantly developed countries. This increase is accompanied by the shift of chronic diseases to the senior population, especially cardiovascular diseases and diabetes type II. Aging mechanisms, mostly post-genetic, comprise among others the Maillard reaction which strongly contributes by several harmful processes to the age-dependent decline of tissue structure and function. Several of these mechanisms were studied in our laboratory at the cellular-molecular level and will be described in this review with respect to their role in aging and age-related pathologies, especially cardiovascular diseases.

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“…HA fragmentation during ECM degradation after acute tissue injury serves the important function of initiating the host innate immune response by providing an essential signal to macrophages and other cell types to produce chemokines that recruit other leukocyte subsets required to achieve tissue injury and to begin restoring tissue integrity [17,[20][21][22]. HA can be depolymerised into small fragments via oxygen radicals and enzymatic degradation by hyaluronidase, β-glucuronidase and hexosaminidase [23][24].…”

Section: Discussionmentioning

confidence: 99%

Small hyaluronan oligosaccharides induce inflammation by engaging both toll-like-4 and CD44 receptors in human chondrocytes

Campo

Avenoso

Campo

et al. 2010

Biochemical Pharmacology

136

104

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HAL is a multi-disciplinary open access archive for the deposit and dissemination of scientific research documents, whether they are published or not. The documents may come from teaching and research institutions in France or abroad, or from public or private research centers. L'archive ouverte pluridisciplinaire HAL, est destinée au dépôt et à la diffusion de documents scientifiques de niveau recherche, publiés ou non, émanant des établissements d'enseignement et de recherche français ou étrangers, des laboratoires publics ou privés. Small hyaluronan oligosaccharides induce inflammation by engaging both toll-like-4 and cd44 receptors in human chondrocytesGiuseppe M. Campo, Angela Avenoso, Salvatore Campo, Angela D'Ascola, Giancarlo Nastasi, Alberto CalatroniTo cite this version: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.Page 1 Adding HA fragments to chondrocyte cultures up-regulated CD44 and TLR-4 expression, activated NF-kB translocation and increased the pro-inflammatory cytokines TNF-α, IL-6 and IL-1β.The addition of a specific CD44 blocking antibody reduced CD44 and all inflammatory cytokine expression as well as protein production. However, cytokine expression remained significantly higher than in untreated chondrocytes. TLR-4 expression was not affected. The treatment with TLR-4 blocking antibody decreased TLR-4 and inflammatory cytokine expression, although cytokine expression was significantly higher than in control cells. CD44 expression was unaffected.The addition of both CD44 and TLR-4 blocking antibodies significantly reduced CD44, TLR-4 and inflammatory cytokine expression.

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Free radical depolymerization of hyaluronan by maillard reaction products

Cited by 76 publications

References 34 publications

Extracellular Superoxide Dismutase Inhibits Inflammation by Preventing Oxidative Fragmentation of Hyaluronan

Extracellular Superoxide Dismutase Inhibits Inflammation by Preventing Oxidative Fragmentation of Hyaluronan

Role of the Maillard reaction in aging and age-related diseases. Studies at the cellular-molecular level

Small hyaluronan oligosaccharides induce inflammation by engaging both toll-like-4 and CD44 receptors in human chondrocytes

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