Endothelial cells stents

Dichek, D.A., Neville, R.F., Zwiebel, J.A., Freeman, S.M., Leon, M.B. and Anderson, W.F. (1989) Seeding of intravascular stents with genetically engineered endothelial cells. Circulation, 80, 1347-1353. 

Hey has been shown to reduce binding of tPA to its endothelial cell receptor, annexin II, in cell cultures (50). Animal studies have indicated that elevated plasma tHcy could cause acquired dysfibrinogenemia, leading to the formation of clots that are abnormally resistant to fibrinolysis (51), Elevated plasminogen activator inhibitor and tHcy in patients with acute coronary syndrome have been shown to be associated with increased risk for major adverse cardiac events (MACE) after successful percutaneous coronary intervention (PCI) and stenting (52), whereas factor V Leiden mutation and lipoprotein (a) were not. 

Jaschke B, Michaelis C, Milz S, et al. Local statin therapy differentially interferes with smooth muscle and endothelial cell proliferation and reduces neointima on a drug-eluting stent platform, Cardiovasc Res 2005 68(3) 483-492. 

Dichek DA, Neville RE Zwiebel JA, et al. Seeding of intravascular stents with genetically engineered endothelial cells. Circulation 1989 80 1347-1353. 

Flugelman MY Virmani R, Leon MB, et al. Genetically engineered endothelial cells remain adherent and viable after stent deployment and exposure to flow in vitro. Circulation Res 1992 70 348-354. 

Scott NA, Candal FJ, Robinson KA, et al. Seeding of intracoronary stents with immortalized human microvascular endothelial cells. Am Heart J 1995 129 860-866. 

Scanning electron micrograph showing continuous endothelial cell coverage of the stent struts after five-day implantation (preclinical study of clinical trial dose BiodivYsio Batimastat Stent). 

While the thiazolidindiones enhance insulin-mediated glucose transport via binding to the peroxisome proliferator-activating receptor (PPAR-y), the presence of this receptor in vascular smooth muscle cells, inflammatory cells, and endothelial cells likely facilitates the drug s ability to inhibit vascular smooth muscle cell proliferation, reduce inflammation, improve dyslipidemia, and, by extension, reduce in-stent restenosis. 

Metallic stents covered with stem cells were proposed as a plausible solution for preventing in-stent thrombosis and restenosis. Raina et al. published in 2014 in vivo results of 152 implanted hTEC covered stents and compared the outcomes with BMS. The preliminary results showed earlier strut coverage with endothelial cells and no increased neointimal proliferation compared to BMS [92],... 

A number of PTMC-based terpolymers have also been studied. Asplund et al. (2006) reported a three-armed P(TMC-co-CL)-PLLA terpolymer as potential stent cover. Random chain scission and homogenous hydrolysis resulted in a loss in mass and molar mass. After 6 weeks of in vitro hydrolysis the molar mass decreased by 54% and the elongation at break dropped from more than 300 to 90%. A medium free cell seeding study showed that endothelial cells adhered well to the polymeric material. Animal study showed very low levels of inflammation, but pronounced neointimal thickening was observed probably due to the premature failure of the material. 

Incorporation of tacrolimus on cardiac drug-eluting stent platforms has not performed as favorably to other drugs. Tacrolimus suppresses smooth muscle and endothelial cell proliferation but is less potent than sirolimus. Unlike sirolimus though, taaolimus does not affect tissue factor and endothelial nitric oxide synthase expression. The Mahoroba DBS applies tacrolimus to a cobalt chromium platform with a PLGA biodegradable polymer. The first-in-man results unfortunately demonstrated failure to prevent neointimal hyperplasia, with a cumulative major adverse cardiac events rate of 23.4% at 6 months [7,8]. 

The coating materials for stents can be broadly classified into four types inorganic materials, polymers, porous metals, and endothelial cells. In this work, we will focus on polymeric coatings, putting special focus on polyurethanes. The main function of the coating is to reduce the incidence of early and late stage thrombosis and restenosis during stent placement. 

As was mentioned before, PU has been extensively studied as a material for cardiovascular applications, and so far has provided encouraging data. The structure of PU consists of a hard segment that provides mechanical strength to the structure, combined with a soft segment that provides elasticity. In-vitro studies have shown that PU-covered stents have greater endothelial cell coverage when compared with PTFE, denoting its better biocompatibility [125]. 

S. Muller-Hiilsbeck, K.P Walluscheck, M. Priebe, J. Grimm, J. Cremer and M. Heller, Experience on endothelial cell adhesion on vascular stents and stent-grafts First in vitro results. Invest. Radiol.37 314-320, 2002. 

Implantation of a polymer device into a vessel or tissue causes a complex inflammatory response inducing adhesive interactions between vascular cells (blood and tissue cells). During stenting, the endothelial layer is partially or completely destroyed. In animal experiments of vascular injury, denudation of endothelial cells results in platelet deposition followed by neointima formation [188-190]. In addition, complete coverage of endothelial cells is associated with attenuation or even stop of the growth of neointima from smooth... 

---