NSAIDS, POLYAMINE-DEPLETION & DEPOLARIZED MEMBRANE POTENTIAL

本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者（PI）可能已经从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。列出的机构是中心的，不一定是研究者的机构。该项目的总体目标是增加对非甾体抗炎药（NSAIDs）胃肠道毒性的分子机制的了解。肠道恢复使用两种肠细胞系的上皮单层进行建模，隐窝细胞系IEC-6及其分化程度更高的衍生物IEC-6- cdx -2。许多实验室先前的研究表明，肠上皮的恢复依赖于Kv1 （KCNA）家族的电压门控K+通道的细胞表达。这些离子通道通过控制膜电位（Em）和下游信号影响细胞在受伤后的迁移。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The overall aim of the project is to increase knowledge about the molecular mechanisms that underly gastrointestinal toxicity of non-steroidal anti-inflammatory drugs (NSAIDs). Intestinal restitution is modeled using epithelial monolayers of two intestinal cell lines, the crypt cell line IEC-6 and its more differentiated derivative IEC-6-Cdx-2. Previous work from a number of laboratories has shown that intestinal epithelial restitution is dependent on the cellular expression of voltage-gated K+ channels from the Kv1 (KCNA) family. These ion channels influence cell migration after wounding through the control of membrane potential (Em) and downstream signals.