NSAIDS, POLYAMINE-DEPLETION & DEPOLARIZED MEMBRANE POTENTIAL

非甾体抗炎药、多胺消耗

• 批准号: 7610456
• 负责人: JAMES D LILLICH
• 金额: $ 3.71万
• 依托单位: KANSAS STATE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-07-01 至 2008-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7610456
• 关键词: Anti-Inflammatory Agents; Anti-inflammatory; Cell Line; Computer Retrieval of Information on Scientific Projects Database; Epithelial; Family; Funding; Grant; Institution; Intestines; Ion Channel; Knowledge; Laboratories; Membrane Potentials; Modeling; Molecular; Numbers; Pharmaceutical Preparations; Polyamines; Research; Research Personnel; Resources; Signal Transduction; Source; Toxic effect; United States National Institutes of Health; Voltage-Gated Potassium Channel; Work; cell motility; crypt cell; gastrointestinal; monolayer

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.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 该项目的总体目的是增加对非甾体类抗炎药（NSAIDS）的胃肠道毒性的分子机制的知识。使用两个肠道细胞系IEC-6及其更分化的衍生化IEC-6-CDX-2的上皮单层对肠道恢复原状。许多实验室的先前工作表明，肠上皮恢复原状取决于来自KV1（KCNA）家族电压门控的K+通道的细胞表达。这些离子通道通过控制膜电位（EM）和下游信号受伤后影响细胞迁移。