NSAIDS, POLYAMINE-DEPLETION & DEPOLARIZED MEMBRANE POTENTIAL

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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.