NSAIDS, POLYAMINE-DEPLETION & DEPOLARIZED MEMBRANE POTENTIAL

非甾体抗炎药、多胺消耗

• 批准号: 7381862
• 负责人: JAMES D LILLICH
• 金额: $ 20.6万
• 依托单位: KANSAS STATE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-07-01 至 2007-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7381862
• 关键词: NSAIDS; POLYAMINE; DEPLETION; DEPOLARIZED; MEMBRANE

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.

该子项目是利用 NIH/NCRR 资助的中心拨款提供的资源的众多研究子项目之一。子项目和研究者 (PI) 可能已从另一个 NIH 来源获得主要资金，因此可以在其他 CRISP 条目中出现。列出的机构是中心的机构，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（NSAID）胃肠道毒性分子机制的了解。使用两种肠道细胞系（隐窝细胞系 IEC-6 及其分化程度更高的衍生物 IEC-6-Cdx-2）的单层上皮来模拟肠道恢复。许多实验室之前的工作表明，肠上皮恢复取决于 Kv1 (KCNA) 家族电压门控 K+ 通道的细胞表达。这些离子通道通过控制膜电位 (Em) 和下游信号来影响受伤后的细胞迁移。