Surface biofunctional modification of coronary artery stents to prevent thrombosis and restenosis formation, as well as accelerate endothelialization, has become a new hot spot. However, bioactive coatings on implants are not yet sufficiently developed for long-term activity, as they quickly lose efficiency in vivo and finally fail. On the basis of a novel time-ordered concept of biofunctionality for vascular stents, heparin/poly l-lysine nanoparticle (NP) was developed and immobilized on a polydopamine-coated titanium surface, with the aim of regulating and maintaining the intravascular biological response within the normal range after biomaterial implantation. An in vitro dynamic release model was established to mimic the blood flow condition in vivo with three phases: (1) An early phase (1-7 days) with release of predominantly anticoagulant and anti-inflammatory substances and to a minor degree antiproliferative effects against smooth muscle cells (SMCs); (2) this is followed by a phase (7-14 days) of supported endothelial cell (ECs) proliferation and suppressed SMC proliferation with persisting high antithrombogenicity and anti-inflammatory properties of the surface. (3) Finally, a stable stage (14-28 days) with adequate biomolecules on the surface that maintain hemocompatibility and anti inflammation as well as inhibit SMCs proliferation and promote ECs growth. In vivo animal tests further confirmed that the NP-modified surface provides a favorable release behavior to apply a stage-adjusted remedy. We suggested that these observations provide important guidance and potential means for reasonable and suitable platform construction on a stent surface.
The change in cytosolic free concentration of calcium ([Ca 2+ ] cyt ) plays a key role in regulating apoptosis in animal cells. In our experiment, we tried to investigate the function of Ca 2+ in programmed cell death (PCD) in tobacco (Nicotiana tobacum, cultivar BY-2) protoplasts induced by salt stress. An obvious increase in [Ca 2+ ] cyt was observed a few minutes after treatment and the onset of a decrease in mitochondrial membrane potential (DW m ) was also observed before the appearance of PCD, pre-treatment of protoplasts with EGTA or LaCl 3 effectively retarded the increase in [Ca 2+ ] cyt , which was concomitant with the decrease in the percentage of cell death and higher DW m , pre-treatment with cyclosporine A (CsA) also effectively retarded the increase in [Ca 2+ ] cyt , the decrease in DW m and the onset of PCD. All these results suggest that Ca 2+ is a necessary element in regulating PCD and the increase in [Ca 2+ ] cyt and the opening of mitochondrial permeability transition pore (MPTP) could promote each other in regulating PCD in tobacco protoplasts induced by salt stress.Abbreviations: AIF -apoptosis inducing factor; ANT -adenine nucleotide translocator; [Ca 2+ ] cytcytosolic free calcium concentration; CsA -cyclosporin A; DCFH-DA -2,7-dichlorohydrofluoroscein diacetate; EB -ethidium bromide; HR -hypersensitive response; MPTP -mitochondrial permeability transition pore; PCD -programmed cell death; PI -propidium iodide; Rh123 -Rhodamine123; ROSreactive oxygen species; DW m -mitochondrial membrane potential
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