Characterization of Annexin A1 Glycan Binding Reveals Binding to Highly Sulfated Glycans with Preference for Highly Sulfated Heparan Sulfate and Heparin

Horlacher, Tim; Noti, Christian; Paz, José L. de; Bindschädler, Pascal; Hecht, Marie-Lyn; Smith, David F.; Fukuda, Minoru; Seeberger, Peter H.

doi:10.1021/bi101121a

Cited by 24 publications

(19 citation statements)

References 49 publications

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“…These annexins can bind to glycosaminoglycans such as heparin and heparan sulfate [Ishitsuka et al, 1998;Capila et al, 2001;Horlacher et al, 2011] in vitro and this interaction may facilitate their anticoagulant activity. It was proposed that heparin interacts with the concave surface of AnxA5 to stabilize self-assembled AnxA5 arrays on membranes and further enhance the anticoagulant activity of AnxA5 [Capila et al, 2001].…”

Section: Discussionmentioning

confidence: 99%

Skin Wound Repair Is Not Altered in the Absence of Endogenous AnxA1 or AnxA5, but Pharmacological Concentrations of AnxA4 and AnxA5 Inhibit Wound Hemostasis

Kreft¹,

Klatt

Strassburger

et al. 2016

Cells Tissues Organs

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Skin injury induces the cell surface exposure of phosphatidylserine (PS) on damaged and dying cells to activate coagulation and repair processes. Annexins can bind to PS and may modulate the healing response. Here, we determine the relevance of annexins for skin wound healing using AnxA1- and AnxA5-deficient mice and recombinant annexins with distinct PS binding properties. Wound inflammation, closure and the formation of granulation tissue were not altered in AnxA1- or AnxA5-deficient mice or after increasing AnxA5 serum concentrations (100 nM) in wild-type mice. Increased serum concentrations (1 µM) of AnxA5 induced massive bleeding, but wound hemostasis was not delayed by AnxA1. Both annexins interact with PS, but only AnxA5 can form 2-dimensional (2D) arrays on the cell surface. The injection of an AnxA5 mutant that binds to PS but lacks the ability of 2D array formation failed to induce bleeding. 2D lattice-forming AnxA4, with high affinity to PS also caused bleeding, while hemostasis was not affected by AnxA8 with low affinity or the AnxA8 mutant with medium affinity for PS and the lack of 2D formation. Increased concentrations of AnxA4 and AnxA5 also delayed coagulation pathway activation in vitro. This effect was attenuated for the AnxA5 mutant as well as for AnxA1 and AnxA8. In conclusion, endogenous AnxA1 and AnxA5 are dispensable for wound hemostasis and repair, but pharmacologically excessive concentrations of AnxA4 and AnxA5 inhibit hemostasis in skin wounds.

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Section: Discussionmentioning

confidence: 99%

Skin Wound Repair Is Not Altered in the Absence of Endogenous AnxA1 or AnxA5, but Pharmacological Concentrations of AnxA4 and AnxA5 Inhibit Wound Hemostasis

Kreft¹,

Klatt

Strassburger

et al. 2016

Cells Tissues Organs

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“…In recent years, studies have shown that anesthetic drugs can inhibit the immune response and control the exudation of inflammatory mediators (Horlacher et al, 2011). Propofol, a type of widely used anesthetic, had been noted for its anti-inflammatory effects.…”

Section: Discussionmentioning

confidence: 99%

Effects of propofol and etomidate pretreatment on glucocorticoid receptor expression following induction of sepsis in rats

Wang

Liu

et al. 2015

Genet. Mol. Res.

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ABSTRACT. The aim of this study was to determine the effect of etomidate and propofol pretreatment on the expression of glucocorticoid receptor and the prognosis of sepsis. The sepsis rat was used as a model. During glucocorticoid treatment, etomidate and propofol were applied alone or together at different time points. Survival curves, glucocorticoid receptor expression in the rat adrenal cortex, and inflammation levels were determined. The outcome of sepsis in rats was evaluated based on the combined utilization of propofol and etomidate. The results indicated that the combined utilization of propofol and etomidate pretreatment could significantly improve the effects of glucocorticoids on rat sepsis. Etomidate was shown to enhance the expression of the glucocorticoid receptor, while propofol was shown to inhibit the inflammatory response. Etomidate was best used immediately after modeling, whereas propofol was most suitable for use during the peak inflammatory reaction. These results demonstrated that anesthetics had 4741 Propofol and etomidate effects on GR in rats with sepsis ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (2): 4740-4748 (2015) the ability to enhance the effect of glucocorticoids in the treatment of sepsis. Etomidate was indicated for use in the early stage of inflammation to enhance expression of the glucocorticoid receptor, while propofol application was indicated at the peak of the inflammatory reaction owing to its strong anti-inflammation effect.

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“…Annexin V, an abundant anticoagulant and phospholipid binding protein binds HS in a calcium ion-dependent manner, binding via two binding sites on opposite faces of the protein [148,149]. The phospholipid binding and calcium-dependent annexin I has been reported as requiring N-and 2-O-sulfate groups for binding [150]. The influence of cations can also vary.…”

Section: Cation Binding To Heparan Sulfate/heparin and Its Effectsmentioning

confidence: 99%

Heparan sulfate and heparin interactions with proteins

Meneghetti

Hughes

Rudd

et al. 2015

J. R. Soc. Interface.

235

225

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Heparan sulfate (HS) polysaccharides are ubiquitous components of the cell surface and extracellular matrix of all multicellular animals, whereas heparin is present within mast cells and can be viewed as a more sulfated, tissuespecific, HS variant. HS and heparin regulate biological processes through interactions with a large repertoire of proteins. Owing to these interactions and diverse effects observed during in vitro, ex vivo and in vivo experiments, manifold biological/pharmacological activities have been attributed to them. The properties that have been thought to bestow protein binding and biological activity upon HS and heparin vary from high levels of sequence specificity to a dependence on charge. In contrast to these opposing opinions, we will argue that the evidence supports both a level of redundancy and a degree of selectivity in the structure-activity relationship. The relationship between this apparent redundancy, the multi-dentate nature of heparin and HS polysaccharide chains, their involvement in protein networks and the multiple binding sites on proteins, each possessing different properties, will also be considered. Finally, the role of cations in modulating HS/heparin activity will be reviewed and some of the implications for structure-activity relationships and regulation will be discussed.

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Characterization of Annexin A1 Glycan Binding Reveals Binding to Highly Sulfated Glycans with Preference for Highly Sulfated Heparan Sulfate and Heparin

Cited by 24 publications

References 49 publications

Skin Wound Repair Is Not Altered in the Absence of Endogenous AnxA1 or AnxA5, but Pharmacological Concentrations of AnxA4 and AnxA5 Inhibit Wound Hemostasis

Skin Wound Repair Is Not Altered in the Absence of Endogenous AnxA1 or AnxA5, but Pharmacological Concentrations of AnxA4 and AnxA5 Inhibit Wound Hemostasis

Effects of propofol and etomidate pretreatment on glucocorticoid receptor expression following induction of sepsis in rats

Heparan sulfate and heparin interactions with proteins

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