NSAIDS, POLYAMINE-DEPLETION & DEPOLARIZED MEMBRANE POTENTIAL

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目及 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 该项目的总体目标是增加有关非甾体抗炎药（NSAID）胃肠道毒性的分子机制的知识。使用两种肠细胞系（隐窝细胞系IEC-6及其更分化的衍生物IEC-6-Cdx-2）的上皮单层对肠恢复进行建模。来自许多实验室的先前工作已经表明，肠上皮恢复依赖于来自Kv 1（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）和下游信号影响创伤后的细胞迁移。

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.