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Table of Contents
Vol. 25, No. 4-5, 2010
Issue release date: March 2010
Section title: Original Paper
Cell Physiol Biochem 2010;25:477–490

Antisense Oligodeoxynucleotide Against Tissue Factor Inhibits Human Umbilical Vein Endothelial Cells Injury Induced by Anoxia-Reoxygenation

Yin J. · Luo X.G. · Yu W.J. · Liao J.Y. · Shen Y.J. · Zhang Z.W.
Division of Hematology, the Second Hospital affiliated to Medical College of Shantou University, Shantou
email Corresponding Author

Dr. Jun Yin, Division of Hematology

the Second Hospital affiliated to Medical College of Shantou University

Dongxia Road North, Shantou, Guangdong Province, 515041 (China)

Tel. + 86 754 8891 5950 (office) or +86 1382 9608 816 (cell phone)

Fax: +86 754 8852 0097, E-Mail jyin@stu.edu.cn

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Aims: The role of antisense oligodeoxynucleotide against tissue factor (aODN/TF) in cultured human umbilical vein endothelial cells (HUVECs) subjected to anoxia-reoxygenation (A/R) was investigated. Methods: HUVECs were divided randomly into control group, A/R group, aODN/TF+A/R group, sense oligodeoxynucleotide (sODN/TF) + A/R group and mismatched oligodeoxynucleotide (mODN/TF) + A/R group, in the latter 3 groups, HUVECs were transfected with aODN/TF, sODN/TF and mODN/TF respectively. HUVECs in all A/R groups underwent 3 hrs of anoxia and followed by 2 hrs of reoxygenation. In order to investigate the potential mechanisms of how increased TF may contribute to A/R injury in HUVECs, another set of HUVECs were incubated with human recombinant active site blocked factor VII (FVIIai) during A/R. Results: After A/R, TF expression at both mRNA and protein level was increased, furthermore, cell viability and the concentrations of SOD, GSH-PX and NO were declined, while LDH, MDA and ET-1 were overproduced (P<0.05 to 0.001 versus control group). In HUVECs of aODN/TF+A/R group, however, TF expression was inhibited, while the declined cell viability and the concentrations of SOD, GSH-PX, NO as well as the enhanced LDH, MDA and ET-1 levels occurred during A/R were ameliorated and reversed effectively (P<0.05 to 0.01 versus those in other A/R groups). The results also showed that ROS was increased and PAR-1, PAR-2, p38 MAP kinase and p42/44 MAP kinase were all activated after A/R (P<0.001 versus HUVECs under normoxia), while FVIIai inhibited the increment of ROS, PAR-1, PAR-2, p38 MAP kinase and p42/44 MAP kinase, and improved the changes of TF:C, MDA, SOD, GSH-PX, cell viability and LDH occurred during A/R (P<0.05 to 0.001 versus HUVECs without FVIIai treatment). Conclusion: Tissue factor plays an important role in the development of HUVECs injury induced by anoxia-reoxygenation, inhibition of TF with antisense oligodeoxynucleotide is an effective approach to ameliorate the damage.

© 2010 S. Karger AG, Basel

Article / Publication Details

First-Page Preview
Abstract of Original Paper

Accepted: January 18, 2010
Published online: March 23, 2010
Issue release date: March 2010

Number of Print Pages: 14
Number of Figures: 0
Number of Tables: 0

ISSN: 1015-8987 (Print)
eISSN: 1421-9778 (Online)

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