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Antisense oligodeoxynucleotide against tissue factor inhibits human umbilical vein endothelial cells injury induced by anoxia-reoxygenation.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Yin, Jun Luo, Xin Guo Yu, Wen Jun Liao, Jing Yuan Shen, You Jin Zhang, Ze Wen |
| Copyright Year | 2010 |
| Abstract | 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. |
| Starting Page | 379 |
| Ending Page | 383 |
| Page Count | 5 |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | https://www.karger.com/Article/Pdf/303053 |
| PubMed reference number | 20332629v1 |
| Alternate Webpage(s) | https://doi.org/10.1159/000303053 |
| DOI | 10.1159/000303053 |
| Journal | Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology |
| Volume Number | 25 |
| Issue Number | 4-5 |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | 3,4-Methylenedioxyamphetamine Anoxia Anoxia-Ischemia, Brain Cell Survival Endothelin-1 Glutathione Human Umbilical Vein Endothelial Cells Oligodeoxyribonucleotides Recombinants Umbilicus (Anatomy) antisense therapy incubated rosiglitazone |
| Content Type | Text |
| Resource Type | Article |
