Chinese Academy of Sciences Key Lab for Biomedical Effects of Nanomaterials and Nanosafety Branch Ⅰ Institute of High Energy Physics, YuQuan Rd 19B, P. O. Box 918, Beijing , China Branch Ⅱ National Center for Nanosciences&Technology No.11 ZhongGuanCun, BeiYiTiao, Beijing , China Tel: Fax: 报告人： Dr. David Leong, National University of Singapore 题 目： Novel effects arising from nanoparticles interactions with endothelial and epithelial cells 时 间： 2014 年 6 月 25 日（星期三）下午 3: 30 地 点：中科院高能物理研究所，主楼 415 会议室 中科院纳米生物效应与安全性重点实验室 纳米技术论坛 ( NS Forum No. XX ) 第 XX 期学术报告会通知 Dr. Leong graduated with a Bachelor of Chemical Engineering and a PhD in Biology from the National University of Singapore. He did his postdoctoral training in the Howard Hughes Medical Institute, University of Pennsylvania and return to his alma mater as a Lee Kuan Yew Postdoctoral Fellow. He later joined the Department of Chemical and Biomolecular Engineering at National University of Singapore as an Assistant Professor in late His research interests includes figuring out biological mechanisms of nanomaterials, nanotoxicology, new biosensors and new nanomedicine. 报告人简介： 主持人：高学云 研究员 电话： 报告摘要 ： Nanoparticles regardless as subjects of nanotoxicity or nanomedicine studies will inevitably interact with endothelial and epithelial cells. In the case of nanomedicine, while these cells are usually not the intended target, nanoparticles first interact with them. It is therefore important to understand the effects of these nanoparticles on these cells. Using generic and commonly found non-decorated nanomaterials like TiO 2, silica, silver, ZnO, hydroxyapatite nanoparticles, we discovered interesting new effects and solved their mechanisms. We discovered that nanoparticles can cause endothelial leakiness (NanoEL) in vitro and in vivo by finding its way into the spaces (adherens junctions) between endothelial cells, disrupts the homophillic interactions of VE-Cadherin and trigger the signaling pathway that leads to micron sized gaps between endothelial cells (Setyawati et al. Nature Comms 2013). We also discovered that nanoparticles can inhibit cell migration by targeting and disrupting microtubules. This increases focal adhesion at the interface of surfaces and transmit to increased cell traction (Tay et al. Nano Letts 2014). We also showed that oxidative stress inducing nanoparticles can be exploited to target cancer cells while sparing normal cells via an vulnerability in p53 defective/deficient cancer cells. Functional p53 pathway in normal cells protect them against the oxidative stress of nanoparticles while cells with deficiencies in the p53 pathway succumb to oxidative stress. This is the first time where targetness of a nanomedicine is purely from a genetic difference between cancer and non-cancer cells (Setyawati et al. Biomaterials 2013). This talk will also discuss about implications of these novel observations to nanotoxicity and nanomedicine.