Uncovering glial dependent mechanisms in neuroinflammation
The Meares lab studies fundamental cellular mechanisms involved in inflammatory and injury responses within the nervous system. Astrocytes, microglia, and oligodendrocytes are critical for nervous system function. These glial cells have essential roles in supporting neurons, defending the CNS from injury and infection, and ensuring efficient neurotransmission. Glial cells are both influenced by and influential in most neurological diseases. Using a variety of biochemical and transcriptomic approaches, we examine how glial cell stress responses augment neuroinflammation in models of neurological conditions including stroke, multiple sclerosis, and neurodegeneration. Our research also examines how glial cells shape the neuroimmune landscape through interactions with other CNS resident and infiltrating immune cells. The overall goal is to identify mechanisms driving glial-dependent inflammation, which may contribute to neuropathology and represent novel therapeutic targets.
Projects
1. PERK dependent mechanisms of neuroinflammation. This project examines the role of the ER stress activated kinase PERK in astrocytes and microglia in ischemic injury and autoimmune neuroinflammation.
2. JAK1 dependent regulation of astrocytes and microglia. Janus Kinase 1 (JAK1) an essential kinase that mediates the intracellular signaling of many cytokines. The project will determine the cell specific function of JAK1 in astrocytes and microglia.
3. T cell dependent reprogramming of glia. T cells infiltrate the CNS in MS and other neurological conditions. This project will investigate the mechanisms and functional effects of T cell interactions with astrocytes and microglia.
4. Up and coming. We have several nascent projects in development. For example, the role of JAK1 in aged glia; how IL-6 is translationally regulated; defining the JAK1 interactome; identifying the PERK and JAK1 dependent non-cell autonomous role of astrocytes and microglia.