Signaling Properties of Hyaluronan Receptors

Turley, Eva A.; Noble, Paul W.; Bourguignon, Lilly Y.W.

doi:10.1074/jbc.r100038200

Cited by 959 publications

(891 citation statements)

References 85 publications

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“…Our recent observation also revealed that CD44 has critical roles in the intracellular and extracellular catabolism of HA mediated by hyaluronidase-1 (Hyal-1) and hyaluronidase-2 (Hyal-2), respectively [16]. In addition, it has been shown that the signaling functions of HA are mediated by CD44 [17]. Consequently, inhibition of HA binding to CD44 could interfere with the turnover and/or function of HA, and might be of therapeutic value in the treatment of various diseases, including osteoarthritis, rheumatoid arthritis and cancer.…”

Section: Introductionmentioning

confidence: 85%

F-19848 A, a Novel Inhibitor of Hyaluronic Acid Binding to Cellular Receptor CD44

et al. 2007

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In the course of our screening for inhibitors of hyaluronic acid (HA) binding to cellular receptor CD44, a novel inhibitor, F-19848 A, was isolated from the cultured broth of the fungus strain Dacrymyces sp. SANK 20204. This compound inhibited the binding of CD44 and HA with an IC 50 value of 23.5 m M and CD44-dependent HA degradation was inhibited with an IC 50 value of 98.6 mM in a cell-based assay. The structure was elucidated by physicochemical properties, analysis of spectral data, and decomposition experiments.

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Section: Introductionmentioning

confidence: 85%

F-19848 A, a Novel Inhibitor of Hyaluronic Acid Binding to Cellular Receptor CD44

et al. 2007

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“…[13,14]. Ankyrin binding is further modulated by RhoA and Rac1, members of the Rho-GTPase family [53]. Activation of both, RhoA and Rac1, is mediated by CD44 itself: CD44/MMP-9 activates TGF-beta [54] which is shown to regulate RhoA activity, rearrangement of the cytoskeleton, and adhesion [55].…”

Section: Intracellular Regionmentioning

confidence: 99%

“…Instead CD44 and Fyn are upregulated in these cells and knock down or inhibition of Fyn results in re-sensitization to Imatinib [151]. Because of known CD44/Fyn association [53], the role of CD44 in this process has to be elucidated further.…”

Section: Experimental Antagonization and Drug Resistancementioning

confidence: 99%

CD44 in hematological neoplasias

2011

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“…Hyaluronan (HA) is bound by a number of ECM and cell surface proteins and is a particularly important component of the ECM [1][2][3][4][5] .HA is involved in moderating many cellular processes, including proliferation, migration, adhesion and apoptosis [6][7][8][9][10][11]. Large molecular mass fragments of HA are involved in space-filling and immunosuppressive roles, whilst smaller HA fragments have been shown to be pro-inflammatory and angiogenic; oligosaccharides may be involved in cell signalling (reviewed in [12]).…”

Section: Introductionmentioning

confidence: 99%

One-electron oxidation and reduction of glycosaminoglycan chloramides: A kinetic study

Sibanda

Parsons

Houée-Levin⊥

et al. 2013

Free Radical Biology and Medicine

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Hypochlorous acid and its acid-base counterpart, hypochlorite ions, produced in inflammatory conditions, may produce chloramides of glycosaminoglycans, the latter being significant components of the extracellular matrix (ECM). This may occur through the binding of myeloperoxidase directly to the glycosaminoglycans.The N-Cl group in the chloramides is a potential selective target for both reducing and oxidising radicals, leading possibly to more efficient and damaging fragmentation of these biopolymers relative to the parent glycosaminoglycans. In this study,the fast reaction techniques of pulse radiolysis and nanosecond laser flash photolysis have been used to generate both oxidizing and reducing radicals to react with the chloramides of hyaluronan (HACl) and heparin (HepCl).The strong reducing formate radicals and hydrated electrons were found to react rapidly with both HACl and HepCl with rate constants of (1-1.7) x 10 8 M -1 s -1 and (0.7-1.2) x 10 8 M -1 s -1 for formate radicals and 2.2 x 10 9 M -1 s and 7.2 x 10 8 M -1 s -1 for hydrated electrons, respectively. The spectral characteristics of the products of these reactions were identical and were consistent with initial attack at the N-Cl groups, followed by elimination of chloride ions to produce nitrogencentred radicals, which re-arrange subsequently and rapidly to produce C-2 radicals on the glucosamine moiety supporting an earlier EPR study by Rees et 3 This is the first study therefore to conclusively demonstrate that reducing radicals react rapidly with glycosaminoglycan chloramides in a site-specific attack at the N-Cl groups, probably to produce a 100 % efficient biopolymer fragmentation process. Although less reactive, carbonate radicals, which may be produced in vivo via reactions of peroxynitrite with serum levels of carbon dioxide ,also appear to react in a highly site-specific manner at the N-Cl group. It is not yet known if such site-specific attacks by this important in vivo species lead to a more efficient fragmentation of the biopolymers than would be expected for attack by the stronger oxidising species, the hydroxyl radical. It is clear however that the N-Cl group formed in inflammatory conditions in the extracellular matrix does present a more likely target for both reactive oxygen species and for reducing species than the N-H groups in the parent glycosaminoglycans. Graphical abstract4

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Signaling Properties of Hyaluronan Receptors

Cited by 959 publications

References 85 publications

F-19848 A, a Novel Inhibitor of Hyaluronic Acid Binding to Cellular Receptor CD44

F-19848 A, a Novel Inhibitor of Hyaluronic Acid Binding to Cellular Receptor CD44

CD44 in hematological neoplasias

One-electron oxidation and reduction of glycosaminoglycan chloramides: A kinetic study

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