巨噬细胞炎性蛋白β3促进大鼠原代神经元和PC12细胞的存活

Background We have previously reported that CCR7 may be neuroprotective in the central nervous system. This study aimed to investigate whether macrophage inflammatory protein 3 beta (MIP-3 beta /CCL19), which is the ligand for CCR7, could promote survival in primary neurons and PC12 cells in vitro. Results We found that within the concentration range of 50 to 200 ng/ml, MIP-3 beta promoted survival in serum-deprived rat primary cortical neurons as well as reduced serum deprivation-induced Bim expression. However, primary cortical neurons were less viable at higher concentrations of MIP-3 beta (≥300 ng/ml). To investigate whether MIP-3 beta acts through its receptor, CCR7, the pEGFP-N1-CCR7 expression vector was constructed and transfected into PC12 cells. We found that MIP-3 beta enhanced survival of PC12 cells that were transfected with pEGFP-N1-CCR7 in serum-free media. In these transfected PC12 cells, MIP-3 beta increased Akt phosphorylation levels at 15 and 60 min this effect was effectively blocked by wortmannin, a specific PI3K inhibitor. ConclusionsThese data suggest that MIP-3 beta promotes survival in serum-deprived rat primary cortical neurons through its receptor, CCR7, and acts as a neurotrophic factor in PC12 cells, most likely via the PI3K/Akt signaling pathway.