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Tropical Journal of Pharmaceutical Research
Pharmacotherapy Group, Faculty of Pharmacy, University of Benin, Benin City, Nigeria
ISSN: 1596-5996
EISSN: 1596-9827
Vol. 13, No. 8, 2014, pp. 1327-1332
Bioline Code: pr14182
Full paper language: English
Document type: Research Article
Document available free of charge

Tropical Journal of Pharmaceutical Research, Vol. 13, No. 8, 2014, pp. 1327-1332

 en Synthetic Polypeptide Derived from Viral Macrophage Inflammatory Protein II Inhibit VEGF Production of Human Glioma U87 Cells through SDF-1α/CXCR4-Mediated AKT Signaling Pathway
Xu, Bo; Tian, Peng; An, Gui-Jie; Liu, Sha; Li, Xiu-Ying; Sun, Han-Xiao; Zhou, Jing-Gung; Ding, Qing & Wei, Pi-Jin

Abstract

Purpose: To evaluate the effect of synthetic polypeptide (N15P) derived from viral macrophage inflammatory protein II (vMIP-II) on the secretion of vascular endothelial growth factor (VEGF) as well as investigate the signaling pathways involved in stromal cell-derived factor-1α (SDF-1α)/CXC Chemokin Receptor 4 (CXCR4) axis-induced VEGF in glioblastoma U87 cells.
Methods: Glioblastoma U87 cells were exposed to SDF-1α, N15P with various concentrations. The expression of CXCR4, SDF-1α and VEGF mRNA were assessed by RT-PCR, while expression level of VEGF was tested by ELISA and protein kinase B (Akt) phosphorylation detected by Western blot.
Results: The results showed that CXCR4, SDF-1α, VEGF are expressed in human glioblastoma U87 cell lines. SDF-1α caused a dose-dependent sensitivity of cell proliferation with a maximum effect at 15 μmole/ml, while N15P decreased cell viability in U87 cells in a dose-dependent manner. SDF-1α stimulated the activation of VEGF, and N15P inhibited the activation of VEGF with or without SDF-1α stimulation. VEGF production in U87 cells was associated with Akt pathway. These changes in intracellular processes were blocked by N15P in a dose-dependent manner.
Conclusion: The results suggest that N15P suppress SDF-1α/CXCR4 Mediated VEGF production through Akt signaling pathway and this may be a potent therapeutic strategy in glioblastoma.

Keywords
Viral macrophage; Inflammatory protein II; Glioblastoma; CXC chemokin receptor 4; Stromal cell-derived factor-1α; Protein kinase B

 
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