Glial scar shown to stimulate growth-inhibitory proteoglycans by astrocytes. Experimental reduction of TGFβ-1 and TGFβ-2 has been shown to partially reduce glial scarring. Interleukins are another potential family of scar-inducing cellular messengers. Particularly, interleukin-1, a protein produced by mononuclear phagocytes, helps to initiate the inflammatory response in astrocytes, leading to reactive astrogliosis and the formation of the glial scar. The cytokine family of glial scar inducers include interferon-γ (IFNγ) and fibroblast growth factor 2 (FGF2). IFNγ has been shown to induce astrocyte proliferation and increase the extent of glial scarring in injured brain models. Further, FGF2 production increases after injury to the
Satellite glial cell found in different cells. Although SGCs express glial fibrillary acidic protein (GFAP) and different S-100 proteins, the most useful marker available today for SGC identification is glutamine synthetase (GS). The levels of GS are relatively low at rest, but they greatly increase if the neuron undergoes axonal damage. Furthermore, SGCs also possess mechanisms to release cytokines, adenosine triphosphate (ATP), and other chemical messengers. Research is currently ongoing in determining the physiological role of satellite glial cells. Current theories suggest that SGCs have a significant role in controlling the microenvironment of the sympathetic ganglia. This is based on the observation that