Abstract
Nitric oxide (NO) is an important signalling molecule involved in haemostasis. NO, present as endogenous S-nitrosothiols, is released by cysteine through a transnitrosation reaction. To exploit this mechanism, cysteine was immobilised onto the different carboxylated polyethylene terephthalate (PET) surfaces using 1-step EDC (1-ethyl-3-(3-dimethylaminopropyl) carbodiimide) crosslinking mechanism. Immobilised cysteine concentration and NO release were dependent on the surface carboxyl density. Stability studies showed that the immobilised cysteine concentration and NO release reduced within 6 h. Immobilisation of cysteine derivatives eliminated the possibility of formation of polycysteine and its electrostatic interaction with the carboxylated PET. The immobilised cysteine concentration did not recover after DTT treatment, eliminating the possibility of disulphide bond formation. Further, cysteine was immobilised using a 2-step EDC crosslinking mechanism. Although the cysteine concentration reduced during stability studies, it recovered upon DTT treatment, indicating that cysteine forms amide bonds with the carboxylated PET and the observed decrease in cysteine concentration is probably due to the formation of disulphide bonds. The haemocompatibility of the cysteine immobilised PET surfaces showed similar results compared to the carboxylated PET. The loss of thiol groups due to the disulphide bond restricts the transnitrosation reaction. Hence, these materials can be used primarily in short-term applications.
Highlights
Nitric oxide (NO) is an important signalling molecule involved in haemostasis
As aminolysis can lead to loss of mechanical strength and glutaraldehyde crosslinking has a risk of cytotoxicity[26,27], other surface modification strategies need to be developed for cysteine immobilisation
The mean cysteine concentration measured on the control, polyethylene terephthalate (PET)-1[COOH]-Cys, PET-2[COOH]-Cys, PET-3[COOH]-Cys, PET-4[COOH]-Cys are 1.1, 4.3, 109.9, 176.0, and 52.7 nmol/cm[2], respectively
Summary
Nitric oxide (NO) is an important signalling molecule involved in haemostasis. NO, present as endogenous S-nitrosothiols, is released by cysteine through a transnitrosation reaction. The developed materials should have similar NO fluxes, for effectively inhibiting platelet adhesion onto their surfaces To overcome these limitations, the generation of NO-releasing materials targeted to utilise endogenous NO donors. Earlier studies have shown that attachment of cysteine significantly decreases the platelet adhesion on the polyurethane and polyethylene terephthalate surfaces through endogenous NO release[24,25]. As aminolysis can lead to loss of mechanical strength and glutaraldehyde crosslinking has a risk of cytotoxicity[26,27], other surface modification strategies need to be developed for cysteine immobilisation To overcome these limitations, cysteine was covalently attached to the carboxylated PET using EDC crosslinking[28].
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