Progression of reactive gliosis and astroglial phenotypic changes following stab wound ‐induced traumatic brain injury in mice

Stab wound results in a focal traumatic brain injury. Following the injury, reactive GFAP+ astrocytes can be clustered in five different reactive phenotypes (I –V) while type 0 astrocytes remain non-reactive. Type V astrocytes exhibit increased cell size, more complex morphology, and reduced expression of homeostatic genes such as glutamine synthetase and aquaporin-4. Conversely, they over-express of the pro-inflammatory molecule C3. Injection of LPS inc reases the abundance of type V astrocytes and NF-κB inhibitor sulfasalazine decreases it. We propose that type V astrocytes represent astrocytes that have undergone pathological remodeling with pro-inflammatory gain of function and diminished homeostatic capacity to support neurons. AbstractAstrocytes are the main homeostatic cells in the central nervous system (CNS) and they have an essential role in preserving neuronal physiology. After brain injury, astrocytes become reactive, and that involves a profound change in the astroglial gene expression program as well as intense cytoskeleton remodeling that has been classically shown by the up-regulation of glial fibrillary acidic protein (GFAP), a pan-reactive gene over-expressed in reactive astrocytes, independently of the type of injury. Using the stab wound rodent model of penetrating traumatic injury in the cortex, we here studied the reactive astroglial morphology and reactive microgliosis in detail at 1, 3, 7, 14, and 28  days post-injury (dpi). By combining immunohis...
Source: Journal of Neurochemistry - Category: Neuroscience Authors: Tags: ORIGINAL ARTICLE Source Type: research