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 tumor necrosis factor α (TNFα) are other cellular factors that work to sensitize neurons to pain. SGCs are present in the PNS in fewer numbers than other more well-known types of glial cells, like astrocytes, but have been determined to affect nociception because of some of their physiological and pharmacological properties. In fact, just like astrocytes, SGCs have the ability to sense and regulate neighboring neuronal activity. First, after a period of nerve cell injury, SGCs are known to up-regulate GFAP and to undergo cell division. They have the ability to release chemoattractants, which are analogous to those released by