Abstract：
:To explore the possible cellular source and mechanism of apolipoprotein E (apoE) expression in mechanical injured neuronal cultures. Primary cultured mouse cortical neurons were subjected into mechanical injury by needle scratching. The conditioned medium of wild type (WT) primary mouse astrocytes was collected and added into cultured injured apoE knockout (KO) neurons. Separately, the conditioned medium of injured apoE KO neurons was collected and added into cultured WT astrocytes. We used a specific inhibitor of extracellular signal-regulated kinase (ERK) to block the possible apoE-associated pathway between injured neurons and astrocytes. The apoE expression levels of the cells and secreted into medium were measured by Western blot, respectively. The apoE expression was increased in neurons after mechanically injury, and the injured neurons uptook the astrocyte-secreted apoE, as well. Furthermore, the injured neurons stimulated astrocytes to express more apoE through the ERK signaling pathway. Mechanical injury triggered the neurons to increasingly synthesized apoE and uptook exogenous apoE, while stimulators released from injured neurons elevated astrocytes in apoE expression and secretion.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Yin C,Zhou S,Jiang L,Sun Xdoi
10.1016/j.neulet.2012.03.023subject
Has Abstractpub_date
2012-04-25 00:00:00pages
77-81issue
1eissn
0304-3940issn
1872-7972pii
S0304-3940(12)00372-2journal_volume
515pub_type
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