It is not clear what effects of CD34-and CD133-specific antibody-coated stents have on reendothelialization and in-stent restenosis(ISR)at the early phase of vascular injury.This study aims at determining the capabilities of different coatings on stents(e.g.gelatin,anti-CD133 and anti-CD34 antibodies)to promote adhesion and proliferation of endothelial progenitor cells(EPCs).The in vitro study revealed that the adhesion force enabled the EPCs coated on glass slides to withstand flow-induced shear stress,so that allowing for the growth of the cells on the slides for 48 h.The in vivo experiment using a rabbit model in which the coated stents with different substrates were implanted showed that anti-CD34 and anti-CD133 antibody-coated stents markedly reduced the intima area and restenosis than bare mental stents(BMS)and gelatin-coated stents.Compared with the anti-CD34 antibody-coated stents,the time of cells adhesion was longer and earlier present in the anti-CD133 antibody-coated stents and anti-CD133 antibody-coated stents have superiority in re-endothelialization and inhibition of ISR.In conclusion,this study demonstrated that anti-CD133 antibody as a stent coating for capturing EPCs is better than anti-CD34 antibody in promoting endothelialization and reducing ISR.
Atherosclerotic prone-rupture plaque is mainly localized in the region of the entrance to the stenosiswith high shear stress and the reasons are largely unknown. Our hypothesis is that such a distributionof cells in atherosclerotic plaque may depend on the angiogenesis. Silastic collars inducedregions of high shear stress (20.6865.27 dynes/cm2) in the upstream flow and low shear stress(12.2561.28 dynes/cm2) in the downstream flow in carotid arteries. Compared with the low shearstress region, plaques in the high shear stress region showed more intraplaque haemorrhaging,less collagen and higher apoptotic rates of vascular smooth muscle cells;endothelial cells (ECs) inthe high shear stress region were characterized with integrity and high endothelial nitric oxidesynthase (eNOS) expression (1570.36345.5% vs 172.9649.9%). The number of intraplaque microvesselsis very high in the high shear stress region (1561.8 n/mm2 vs 3.560.4 n/mm2), and themicrovessels in the plaque show ECs were abnormal, with membrane blebs, intracytoplasmic vacuolesand leukocyte infiltration. Our current study reveals that the integrity of the endothelium andthe vulnerability of atherosclerotic plaques are simultaneously localized in high shear stress regions,and we provide evidence for the first time that microvessels in the intraplaque maybe responsiblefor rupture-prone plaque formation in the high shear stress region.
Juhui QiuDaoxi LeiJianjun HuTieying YinKang ZhangDonghong YuGuixue Wang
Docetaxel(DTX),a paclitaxel analogue,can efficiently inhibit proliferation of vascular smooth muscle cells and has broadly been used as an antiangiogenesis drug.However,as a candidate drug of drug-eluting stent,the effects of DTX on human umbilical vein endothelial cells(HUVECs)are still not well understood.Herein,we investigated the effects of DTX on proliferation,apoptosis,adhesion,migration and morphology of HUVECs in vitro.We found that DTX had the cytostatic and cytotoxic effects at low and high concentrations,respectively.DTX could inhibit the proliferation and migration of HUVECs,induce HUVECs apoptosis,delay HUVECs adhesion and decrease spreading area and aspect ratio of individual cells.The signaling pathway that DTX led to the migration inhibition,adhesion delay and shape change of HUVECs is the VE-cadherin mediated integrin b1/FAK/ROCK signaling pathway.The study will provide a theoretical basis for the clinical application of DTX.
Tingzhang HuChun YangMeiling FuJiali YangRolin DuXiaolin RanTieying YinGuixue Wang
Rupture of atherosclerotic plaques causing thrombosis is the main cause of acute coronary syndrome and ischemic strokes.Inhibition of thrombosis is one of the important tasks developing biomedical materials such as intravascular stents and vascular grafts.Shear stress(SS)influences the formation and development of atherosclerosis.The current review focuses on the vulnerable plaques observed in the high shear stress(HSS)regions,which localizes at the proximal region of the plaque intruding into the lumen.The vascular outward remodelling occurs in the HSS region for vascular compensation and that angiogenesis is a critical factor for HSS which induces atherosclerotic vulnerable plaque formation.These results greatly challenge the established belief that low shear stress is important for expansive remodelling,which provides a new perspective for preventing the transition of stable plaques to high-risk atherosclerotic lesions.
Yi WangJuhui QiuShisui LuoXiang XieYiming ZhengKang ZhangZhiyi YeWanqian LiuHans GregersenGuixueWang
