RESUMO
Objective:To investigate the function and mechanism of CXC chemokine receptor 7 (CXCR7) in neuronal cells of ischemic stroke.Methods:The expression of CXCR7 in human neuroblastoma SH-SY5Y cells was interfered by small interfering RNA (si-RNA) technique. Oxygen-glucose deprivation/reoxygenation (OGD/R) injury model was constructed in SH-SY5Y cells. CXCR7 protein expression and cell cycle were detected by flow cytometry (FCM). The protein expression of CXCR7 and Akt signaling pathway was detected by Western blotting.Results:After 6 hours of OGD/R, the expression of CXCR7 was significantly decreased compared with OGD/R 0 hour (CXCR7/GAPDH: 0.483±0.098 vs. 1.000±0.000 by Western blotting and 0.686±0.0524 vs. 1.000±0.000 by FCM, both P < 0.01), cell cycle arrest in G0/G1 phase (1.190±0.040 vs. 1.000±0.000, P < 0.01). After CXCR7 si-RNA interference with SH-SY5Y cells, OGD/R was constructed again for 6 hours. Compared with negative control group (si-NC group) under the same environment, the expression of CXCR7 and phosphorylated Akt (p-Akt) was significantly decreased (CXCR7/GAPDH: 0.471±0.051 vs. 1.000±0.000, p-Akt/GAPDH: 0.616±0.027 vs. 1.000±0.000, both P < 0.001) and cell cycle arrest in G0/G1 phase (1.105±0.033 vs. 1.000±0.000, P < 0.05). Conclusion:The CXCR7 could regulate the cycle of neuronal cells in ischemic stroke through Akt signaling pathway, which has a protective effect on neuronal cells.
RESUMO
Objective:To explore the effect of upregulating CXC-chemokine receptor 7 (CXCR7) in endothelial progenitor cells (EPCs) on angiogenesis after cerebral ischemia-reperfusion injury. Methods:EPCs were isolated and cultured from human umbilical cord blood and identified. Then, the EPCs were transfected with CXCR7 overexpression lentiviral vector, and the expression of CXCR7 was identified with real-time PCR and Western blotting. The tube-like structure formation and apoptosis of EPCs under oxidized low density lipoprotein (ox-LDL) were detected with tube-like structure formation test and Annexin V/PI staining. Cerebral ischemia-reperfusion injury model in rats was established, and the qualified model rats were randomly divided into three groups after 24 hours reperfusion: PBS group (n = 12) was injected with phosphate buffers through tail vein, control group (n = 12) was injected the EPCs infected with control lentiviral vector, and CXCR7 group (n = 12) was injected with EPCs infected with CXCR7 overexpression lentiviral vector. Neurological function scores were determined seven and 14 days after transplantation. The cerebral infarct volume was measured, the number of GFP-positive cells in the ischemic site and the density of capillary were observed. Results:The expression of CXCR7 in EPCs increased after transfection (P < 0.01). Overexpression of CXCR7 improved tube formation and reduced apoptosis of EPCs under ox-LDL (P < 0.05). Compared with PBS and control groups , neurological function improved in CXCR7 group, with less infarct volume, more GFP-positive cells and density of capillary (P < 0.05). Conclusion:Up-regulating CXCR7 can improve the survival and angiogenesis of EPCs, and improve the repair of cerebral ischemia-reperfusion injury.
RESUMO
AIM:To evaluate the expression level of CXC chemokine receptor 7 (CXCR7) in atherosclerotic apolipoprotein E-deficient ( ApoE-/-) mice induced by high-fat diet ( HFD) and the effects of atorvastatin on it .METH-ODS:ApoE-/-male mice (8-week-old) were used and were randomly divided into 3 groups following 1-week normal ro-dent diet:normal diet control (NDC) group , HFD group and HFD+statins (HFD+Sat) group.HE staining and oil red O staining were used to observe the atherosclerotic lesion burdens in the aortas .The expression of CXCR7 on the aortas was detected by Western blot and immunohistochemistry .The expression of Akt and endothelial nitric oxide synthase ( eNOS) in the aorta was determined by Western blot .RESULTS: Few lesions were found in the aortas in NDC group .Apparent atherosclerotic plaque burdens were seen in HFD group and HFD +Sat group, while the atherosclerotic plaque burdens in HFD+Sat group were notably reduced compared with HFD group .The protein levels of CXCR7, eNOS and Akt in aorta in HFD group and HFD+Sat group were significantly decreased compared with NDC group , while those in HFD+Sat group were increased compared with HFD group .The protein level of p-eNOS in the aorta and the concentration of NO in the plas-ma in HFD group were decreased compared with NDC group and HFD +Sat group.CONCLUSION: In ApoE-/-mice, HFD increases the lipid level and promotes the development of atherosclerosis by downregulating the expression of CXCR 7, Akt and eNOS.Atorvastatin reverses the above effect of hypercholesterolemia on the expression of CXCR 7, Akt and eNOS, thus playing the role in treating atherosclerosis .