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 physiological properties, such as the presence of neurotransmitter transporters and the expression of glutamine synthetase. However, there are distinguishing factors that put SGCs in their own distinct category of glial cells. SGCs most often surround individual sensory and parasympathetic neurons with a complete, unbroken sheath while most neurons of sympathetic ganglia lack a completely continuous SGC sheath, allowing for limited direct exchange of materials between the extracellular space of the neuron and the space within the connective tissue where the SGCs are situated. Furthermore, gap junctions exist between SGCs in the sheaths of adjacent neurons as well as between SGCs