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 in nociception. Various neuronal receptors present on SGCs have been named as participants in ATP-evoked pain signals, particularly the homomultimer P2X3 and the heteromultimer P2X2/3 purinoceptors. In general, the P2X family of receptors responds to neuronally released ATP. Each of the P2X subtypes are found in sensory neurons with the exception of the P2X7 receptor, which is selectively expressed by glial cells, including SGCs. The receptor has been implicated in the release of interleukin IL-1β from macrophages or microglia and astrocytes. The receptor likely has a part in the cascade of events that end with inflammation and neuropathic pain. It