Indexed by Science Citation Index (SciSearch), International Pharmaceutical Abstract, Chemical Abstracts, Embase, Index Copernicus, EBSCO, African Index Medicus, JournalSeek, Journal Citation Reports/Science Edition, Directory of Open Access Journals (DOAJ), African Journal Online, Bioline International, Open-J-Gate

ISSN: 1596-5996 (print); 1596-9827 (electronic)-


Home | Back Issues | Current Issue | Review manuscript | Submit manuscript

 
 

This Article

 

Abstract

 

Full-Text (PDF)

 

Table of contents

 

Comments

 

Letters

 

Comments to Editor

 

e-mail Alert

 

Sign Up

 

Original Research Article


 

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

 

Bo Xu, Peng Tian, Gui-Jie An, Sha Liu, Xiu-Ying Li, Han-Xiao Sun*, Jing-Gung Zhou, Qing Ding and Pi-Jin Wei

Institute of Genomic Medicine, College of Pharmacy, Jinan University, Guangzhou 510632, China

 

*For correspondence: Email: sunhx718@163.com; Tel: +86 - 020-38375022

 

Received: 18 March 2014                                                                      Revised accepted: 3 July 2014

 

Tropical Journal of Pharmaceutical Research, August 2014; 13(8): 1327-1332

http://dx.doi.org/10.4314/tjpr.v13i8.18   

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

Copyright@2002-2010. Pharmacotherapy Group, Faculty of Pharmacy, University of Benin, Benin City. All rights reserved.

Powered by Poracom E-mail: jmanager@poracom.net