Role of AKAPs in Microglial Mediated Inflammation Post CNS Injury

Saturday, February 13, 2016
Gabrielle Petroka, University of Miami, Coral Gables, FL
Cyclic AMP levels decrease after damage to the central nervous system and it is well established that AKAPs (A-kinase Anchoring Proteins) play a major role in orchestrating localized cAMP levels in the cell. AKAPs, which are part of multiprotein signaling network, provide a framework point by which enzymes and their resultant signals are collected and spatially directed within cells. AKAPs are also known to cluster proteins and their substrates as well as regulate ion channels. There are 43 known AKAPs to date, however, due to their wide array of abilities and locations throughout the cell, there is still a lot unknown regarding their functions. Elucidation of AKAP signaling in microglia may help us better understand the functions of microglia involvement after nervous system injury. Specifically, the aim of this study is to determine via Western Blot the degree to which AKAPs may be expressed after injury and to evaluate the localization using Immunocytochemistry. Our hypothesis is that certain AKAPs are involved in regulating cAMP levels post-CNS injury. Initial results from immunoblotting show three AKAPs being expressed post-activation – AKAP-10, 7, and 95 – and potential regulation of these clustering proteins. Immunocytochemistry results revealed that AKAP95 may be downregulated in the nucleus post-activation. The emergence of these particular AKAPs post-activation appears to support our hypothesis; however further testing in tissue and primary culture is necessary.