OECs Prevented Neuronal Cells from Apoptosis Partially Through Exosome-derived BDNF.

It is known that neurotrophic factors are a major source of the neuroprotective effects of olfactory ensheathing cells (OECs). However, the form of neurotrophic factors that originate from OECs is not fully understood. Our previous study demonstrated that OECs could secrete exosome (OECs-Exo), which provided neuroprotection by switching the phenotype of macrophages/microglia. Considering that exosomes could also be taken up by neurons, we explored the direct effect of OECs-Exo on neuronal survival and the underlying mechanism. Electron microscopy, nano-traffic analysis, and Western blotting were applied to identify the OECs-Exo. The effect of OECs-Exo on neuronal survival was tested by flow cytometry and TUNEL staining. Western blotting and ELISA were used to detect neurotrophic factors in purified OECs-Exo. We first isolated OECs-Exo and found that OECs-Exo exerted protective effects on neuronal survival in response to TNF-α challenge. Brain-derived neurotrophic factor (BDNF) was then identified in OECs-Exo, and its receptor TrkB in neurons was activated by OECs-Exo treatment. Furthermore, we demonstrated that OECs prevented TNF-α-induced apoptosis in neurons partially through exosome-derived BDNF. Our data showed that OECs attenuated TNF-α-induced apoptosis in neurons partially through OEC-Exo-derived BDNF, which might provide a novel strategy for the neuroprotective effect of OEC-Exo-based treatment.

[Effect of chronic enhanced external counterpulastion on gene expression profiles of arterial endothelial cells of pigs fed with high-cholesterol diet].

OBJECTIVE: To investigate the effect of chronic enhanced external counterpulastion (EECP) on gene expression profiles of arterial endothelial cells (ECs) of pigs fed with high-cholesterol diet. METHODS: Eight male pigs were fed with high-cholesterol diet for 12 weeks to induce arteriosclerosis and subjected to EECP for accumulative 36 h (2 h every other day for 18 sessions). Another 8 pigs on cholesterol-enriched diet and 6 normally fed pigs served as the arteriosclerosis model group and normal control group, respectively, and the high-cholesterol diet was maintained until the end of EECP treatment. The coronary artery was then isolated for transmission electro microscopy, and the abdominal aorta was observed using Sudan III staining. The gene expression profiles in ECs from the thoracic aorta using cDNA microarrays. RESULTS: Macrophages and foam cells were detected beneath the ECs in the coronary artery of pigs in the model group, but not in the other two groups. The ratios of Sudan III-positive area in the celiac aorta were significantly lower in normal control and EECP groups than in the model control group (P<0.05). Compared with the normal control group, the gene expressions of integrins-beta1 and CTGF were up-regulated in the model group. Compared with the model group, the expressions of integrins-beta1, CTGF and VCAM-1 were down-regulated and eNOS up-regulated in EECP group. CONCLUSION: Chronic EECP may reduce endothelial injury, down-regulate the gene expression level of integrin-beta1, CTGF and VCAM-1, lower cholesterol uptake and attenuate arterial endothelial inflammation to protect the pigs fed with high-cholesterol diet from arteriosclerosis.