Protection against hypoxic-ischemic injury in transgenic mice overexpressing Kir6.2 channel pore in forebrain

Lisa Héron-Milhavet, Yang Xue-Jun, Susan J. Vannucci, Teresa L. Wood, Lisa B. Willing, Bethel Stannard, Catalina Hernandez-Sanchez, Charles Mobbs, Anne Virsolvy, Derek LeRoith

Research output: Contribution to journalArticlepeer-review

38 Scopus citations

Abstract

The role of the K-ATP channel pore-forming subunit Kir6.2 on protection from cerebral hypoxic-ischemic injury was assessed in transgenic mice overexpressing normal Kir6.2 or a dominant negative form (AFA) of this subunit in the forebrain. The resulting mice overexpress either the Kir6.2 or the AFA transgene mainly in the cerebral cortex and hippocampus. The Kir6.2 transgenic mice are resistant to hypoxic-ischemic injury showing a decreased region of cortical damage as compared to the dominant negative AFA and the wild-type mice. Moreover, the overexpression of Kir6.2 allowed an important silencing of the neurons present in forebrain regions thus protecting them from ischemic injury. Interestingly, the phenotype observed in Kir6.2 transgenic mice was observed without increased sulfonylurea binding. Taken together, these results indicate that the transgenic overexpression of Kir6.2 in forebrain significantly protects mice from hypoxic-ischemic injury and neuronal damage seen in stroke.

Original languageEnglish
Pages (from-to)585-593
Number of pages9
JournalMolecular and Cellular Neurosciences
Volume25
Issue number4
DOIs
StatePublished - Apr 2004

Fingerprint

Dive into the research topics of 'Protection against hypoxic-ischemic injury in transgenic mice overexpressing Kir6.2 channel pore in forebrain'. Together they form a unique fingerprint.

Cite this