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
Human Endogenous Retrovirus-W influence the expression of HERV-W. Through qPCR methods and infection of cells with influenza and human herpes simplex 1 it was found that HERV-W has a heighted expression in a cell-specific manner when infected but no mechanism was revealed. Also, when these cells are placed in stressful environments such as serum deprivation similar and increased expression of HERV-W is also recorded. This suggests that HERV-W is modulated by environmental effects. Another study also infected cells with influenza to show that this virus can transactivate HERV-W elements. Influenza produces Glial Cells missing 1 (GCM1) that can act as an enhancer to