Mathematical modeling of material-induced blood plasma coagulation

Guo, Zhenghong; Bussard, Karen M.; Chatterjee, Kaushik; Miller, Rachel E.; Vogler, Erwin A.; Siedlecki, Christopher A.

doi:10.1016/j.biomaterials.2005.06.021

Cited by 51 publications

(86 citation statements)

References 54 publications

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“…Finally, we found that autohydrolysis (FXII À! FXIIa 2FXIIa) was a facile reaction in neatbuffer solution but insignificant in plasma [11,26]. Needless to say perhaps, these new findings are quite contrary to expectations based on the traditional understanding of autoactivation biochemistry briefly outlined above.…”

Section: Introductionmentioning

confidence: 73%

“…Clearly, an improved understanding of the events leading to thrombus formation on biomaterials is needed that will define new bioengineering routes to hemocompatibility. An approach we have taken has been to simplify the problem down to the minimum essential unit of study [6][7][8][9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

“…We have pursued studies of whole-plasma coagulation seeking to resolve detailed relationships among biomaterial surface chemistry, energy, and the propensity to activate the intact plasma coagulation cascade [6][7][8][9][10][11][12]. Results of these 'holistic' studies [11] have motivated us to serially simplify the focus of investigation from whole plasma, to a group of coagulation proteins, to finally purified enzymes of the cascade as a means of comparing activation of the pieces to activation of the whole [10,11,25]. In very brief summary, we found that potentiation of the intrinsic pathway in vitro leads to bolus release of thrombin (FIIa) in concentration proportion to the intensity of activation as measured by procoagulant surface area or surface energy (hydrophilicity, water wettability).…”

Section: Introductionmentioning

confidence: 99%

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Competitive-protein adsorption in contact activation of blood factor XII☆☆☆

Zhuo¹,

Siedlecki

Vogler

2007

Biomaterials

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Contact activation of blood factor XII (FXII, Hageman factor) is moderated by the protein composition of the fluid phase in which FXII is dissolved. Solution yield of FXIIa arising from FXII contact with hydrophilic activating particles (fully water-wettable glass) suspended in a protein cocktail is shown to be significantly greater than that obtained under corresponding activation conditions in buffer solutions containing only FXII. By contrast, solution yield of FXIIa arising from FXII contact with hydrophobic particles (silanized glass) suspended in protein cocktail is sharply lower than that obtained in buffer. This confirms that contact activation is not specific to anionic hydrophilic surfaces as proposed by the accepted biochemistry of surface activation. Rather, contact activation in the presence of proteins unrelated to the plasma coagulation cascade leads to an apparent specificity for hydrophilic surfaces that is actually due to a relative diminution of activation at hydrophobic surfaces and an enhancement at hydrophilic surfaces. Furthermore, the rate of FXIIa accumulation in whole-plasma and buffer solution is found to decrease with time in the continuous presence of activating surfaces, leading to a steady-state FXIIa yield dependent on the initial FXII solution concentration for both hydrophilic and hydrophobic procoagulant particles suspended in either plasma, protein cocktail, or buffer. These results strongly suggest that activation competes with an autoinhibition reaction in which FXIIa itself inhibits FXII-->FXIIa. Experimental results are modeled using a reaction scheme invoking FXII activation and autoinhibition linked to protein adsorption to procoagulant surfaces, where FXII activation is presumed to proceed by either autoactivation (FXII-->surface-->FXIIa) and autohydrolysis (FXII-->FXIIa-->2FXIIa) in buffer solution or autoactivation and reciprocal activation (kallikrein-mediated hydrolysis) in plasma. FXII adsorption competition with other proteins in the fluid phase is proposed to affect the balance of activation and autoinhibition, leading to the observed moderation of FXIIa yield.

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Section: Introductionmentioning

confidence: 73%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Competitive-protein adsorption in contact activation of blood factor XII☆☆☆

Zhuo¹,

Siedlecki

Vogler

2007

Biomaterials

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“…The intrinsic cascade is initiated when contact is made between blood and surfaces. 27,28 The extrinsic pathway is initiated upon vascular injury which leads to exposure of tissue factor (TF) (also known as factor III). 27 Classical biochemistry of the intrinsic clotting pathway suggests that a ''pro-coagulant stimulus,'' starting with exposure of plasma to a test surface, potentiates a cascade of events that culminate into the release of thrombin (Factor IIa).…”

Section: Plasma Recalcification Profilesmentioning

confidence: 99%

Hemocompatibility evaluation of poly(diol citrate) in vitro for vascular tissue engineering

Motlagh

Allen

Hoshi

et al. 2007

J Biomedical Materials Res

128

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One of the ongoing challenges in tissue engineering is the synthesis of a hemocompatible vascular graft. Specifically, the material used in the construct should have antithrombogenic properties and support the growth of vascular cells. Our laboratory has designed a novel biodegradable, elastomeric copolymer, poly(1,8-octanediol citrate) (POC), with mechanical and degradation properties suitable for vascular tissue engineering. The hemocompatibility of POC in vitro and its ability to support the attachment and differentiation of human aortic endothelial cell (HAEC) was assessed. The thrombogenicity and inflammatory potential of POC were assessed relative to poly(l-lactide-co-glycolide) and expanded poly(tetrafluoroethylene), as they have been used in FDA-approved devices for blood contact. Specifically, platelet aggregation and activation, protein adsorption, plasma clotting, and hemolysis were investigated. To assess the inflammatory potential of POC, the release of IL-1beta and TNF-alpha from THP-1 cells was measured. The cell compatibility of POC was assessed by confirming HAEC differentiation and attachment under flow conditions. POC exhibited decreased platelet adhesion and clotting relative to control materials. Hemolysis was negligible and protein adsorption was comparable to reference materials. IL-1beta and TNF-alpha release from THP-1 cells was comparable among all materials tested, suggesting minimal inflammatory potential. POC supported HAEC differentiation and attachment without any premodification of the surface. The results described herein are encouraging and suggest that POC is hemocompatible and an adequate candidate biomaterial for in vivo vascular tissue engineering.

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“…Autohydrolysis of FXII is a putative "self-reaction", where FXII is a substrate for the FXII enzyme. Mathematical models of the intrinsic pathway of blood-plasma coagulation suggest that autohydrolysis is an insignificant reaction in plasma, but significant in pure buffer solutions of FXII and aFXIIa [26,38].…”

Section: Discussionmentioning

confidence: 99%