The absorption of apolipoprotein E by damaged neurons facilitates neuronal repair.

Traumatic brain injury (TBI) is one of the common diseases diagnosed in departments of neurosurgery. Apolipoprotein E (apoE) can improve the prognosis of TBI. In this study, we aimed to explore the effect of apoE in mechanically damaging neurons as well as its underlying molecular mechanism. Western blot analysis and immunofluorescence assay was performed to detect the expressions of associated proteins. The expressions of apoE, p38, and phosphorylation of P38 were increased in mechanically injured neurons compared with those of the non-injured ones. Neurons transfected into silencing apoE had no clear difference in the expression of apoE between injured and non-injured neurons. However, in the injured neurons, silencing apoE could significantly decrease apoE and p-P38 expressions. Oligodendrocytes were cultured in the medium collected from mechanically damaged si-apoE neurons. Furthermore, we found that mechanically injured si-apoE neurons could absorb the secreted apoE from the oligodendrocyte medium of the injured si-apoE-neuron, along with increasing of p-P38 expression at 24 h. The p38 MAPK inhibitor BIRB 796 almost did not affect the apoE expression at 24 h, but significantly reduced the p-P38 level at 24 and 72 h in injured si-apoE neurons cultured with oligodendrocyte medium of the injured si-apoE-neurons. Moreover, our result showed that neuronal repair effects in normal neurobasal medium (lowest levels of apoE and p-P38) and BIRB 796 medium (low level of p-P38) were more slow than those in the oligodendrocyte medium of the injured si-apoE-neurons. To conclude, our data demonstrated that mechanical injury of neurons stimulated oligodendrocytes to secrete apoE. The injured neurons could absorb secreted apoE. The expression of apoE contributed to the activation of p38 MAPK, which facilitated neuron repair.

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