Biological Mechanisms
The changes of astrogliosis are regulated in a context-specific manner by specific signaling events that have the potential to modify both the nature and degree of those changes. Under different conditions of stimulation, astrocytes can produce intercellular effector molecules to alter their expression of molecules in cellular activities of cell structure, energy metabolism, intracellular signaling, and membrane transporters and pumps. Reactive astrocytes respond in accordance with different signals and impact neural function. Molecular mediators are released by neurons, microglia, oligodendrocyte lineage cells, endothelia, leukocytes, and other astrocytes in the CNS tissue, in response to insults ranging from subtle cellular perturbations to intense tissue injury and cell death. The effects can range from regulation of blood flow to provision of energy to synaptic function and plasticity.
A few of the known signaling molecules and its effects are understood in the context of reactive astrocytes responding to different phases of insults.
Upregulation of GFAP production, which can be induced by FGF, TGFB, and ciliary neurotrophic factor (CNTF), is a classic marker for reactive astrocytosis. Where there is an increase in Intermediate filaments GFAP and vimentin, axons will not regenerate. Paradoxically, increase in GFAP production is also specific to minimizing the lesion size and reducing the risk for autoimmune encephalomyelitis and stroke.
The presence of astrocyte glutamate transporters are associated with reducing seizures and further neurodegeneration. Astrocyte water channel AQP4 plays a role in cytotoxic edema and aggravate outcome after stroke. Astrocyte gap junction protein Cx43 contributes to the neuroprotective effect of preconditioning to hypoxia.
Read more about this topic: Astrogliosis
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