Apolipoprotein E knockout induced inflammatory responses related to microglia in neonatal mice brain via astrocytes.

Abstract

More and more evidences suggestted that ApoE plays an important role in modulating the systemic and central nervous inflammatory responses. However, there is a lack of exacted mechanism of ApoE. In this study, we aimed to investigate whether apolipoprotein E (ApoE) induced inflammatory responses and apoptosis in neonatal mice brain from ApoE deficient (ApoE(-/-)) and wildtype (WT). Compared to control group, the microglia cell from ApoE(-/-) mice showed more severe inflammation and cell death such as iNOS and IL-1β. Furthermore, anti-inflammatory such as TGF-β, IL-10 from microglia and astrocytes in ApoE(-/-) mice were decreased. On the other way, TGF-β from astrocytes can inhibit inflammation factors secretion from microglia. Our findings suggested that the anti- inflammation factor such as IL-10 mainly from microglia and TGF-β mainly from astrocyte is significant decreased after Loss of ApoE function in ApoE(-/-) mice which induced severe inflammation. Furthrtmore, anti- inflammation factor such as IL-10 and TGF-β Therefore, we conclude that apolipoprotein E knockout induced inflammatory responses related to microglia in neonatal mice brain via astrocytes.