| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 6262173 | Brain Research Bulletin | 2011 | 7 Pages |
Neuronal survival can be influenced by activated microglia, but limited evidence exists on the effects of paracrine signaling from brain microvascular endothelial cells (BMECs) on microglial action. Therefore, we examined the effects of normal BMECs conditioned medium (BMECs-CM) on activated microglia induced by pro-inflammatory cytokine macrophage inflammatory protein-1beta (MIP-1β), a chemokine that released from ischemic BMECs and has been proved to stimulate microglial proliferation. Our results showed that BMECs-CM inhibited the proliferation and transmigration of microglia induced by MIP-1β. Moreover, BMECs-CM significantly suppressed the expression of the MIP-1β receptor, CCR5, and the phosphorylation of p38 and JNK (P < 0.05). These findings suggest that BMECs-CM could inhibit MIP-1β-induced microglial activation. Future therapeutic strategies that prioritize the early recovery of BMECs could be beneficial for microglial inhibition and further increase neuronal survival.
⺠The effect of brain microvascular endothelial cells (BMECs) paracrine on microglia is unstudied. ⺠MIP-1β was increase and up-regulated in ischemic BMECs conditioned medium and BMECs. ⺠Culture medium from BMECs was shown to reduce microglial activation in inflammation. ⺠The receptor for MIP-1β, a pro-inflammatory cytokine, was downregulated. ⺠Prioritizing BMECs recovery could inhibit microglia and increase neuronal survival.
