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Angiopoietin-1 and Vascular Endothelial Growth Factor Regulation of Leukocyte Adhesion to Endothelial Cells
| Content Provider | Scilit |
|---|---|
| Author | Ismail, Hodan Mofarrahi, Mahroo Echavarria, Raquel Harel, Sharon Verdin, Eric Lim, Hyung W. Jin, Zheng-Gen Sun, Jianxin Zeng, Huiyan Hussain, Sabah N. A. |
| Copyright Year | 2012 |
| Description | Journal: Arteriosclerosis, thrombosis, and vascular biology Objective— Vascular endothelial growth factor (VEGF) promotes leukocyte adhesion to endothelial cells (ECs). Angiopoietin-1 (Ang-1) inhibits this response. Nuclear receptor-77 (Nur77) is a proangiogenic nuclear receptor. In the present study, we assessed the influence of Ang-1 and VEGF on Nur77 expression in ECs, and evaluated its role in Ang-1/VEGF-mediated leukocyte adhesion. Methods and Results— Expression of Nur77 was evaluated with real-time polymerase chain reaction and immunoblotting. Adhesion of leukocytes to ECs was monitored with inverted microscopy. Nur77 expression or activity was inhibited using adenoviruses expressing dominant-negative form of Nur77, retroviruses expressing Nur77 in the antisense direction, and small interfering RNA oligos. Both Ang-1 and VEGF induce Nur77 expression, by >5- and 30-fold, respectively. When combined, Ang-1 potentiates VEGF-induced Nur77 expression. Ang-1 induces Nur77 through the phosphoinositide 3-kinase and extracellular signal-regulated protein kinase 1/2 pathways. VEGF induces Nur77 expression through the protein kinase D/histone deacetylase 7/myocyte enhancer factor 2 and extracellular signal-regulated protein kinase 1/2 pathways. VEGF induces nuclear factor-kappaB transcription factor, vascular cell adhesion molecule-1, and E-selectin expressions, and promotes leukocyte adhesion to ECs. Ang-1 inhibits these responses. This inhibitory effect of Ang-1 disappears when Nur77 expression is disrupted, restoring the inductive effects of VEGF on adhesion molecule expression, and increased leukocyte adhesion to ECs. Conclusion— Nur77 promotes anti-inflammatory effects of Ang-1, and functions as a negative feedback inhibitor of VEGF-induced EC activation. |
| Related Links | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4183139/pdf https://www.ahajournals.org/doi/pdf/10.1161/ATVBAHA.112.251546 |
| Ending Page | 1716 |
| Page Count | 10 |
| Starting Page | 1707 |
| ISSN | 10795642 |
| e-ISSN | 15244636 |
| DOI | 10.1161/atvbaha.112.251546 |
| Journal | Arteriosclerosis, thrombosis, and vascular biology |
| Issue Number | 7 |
| Volume Number | 32 |
| Language | English |
| Publisher | Ovid Technologies (Wolters Kluwer Health) |
| Publisher Date | 2012-07-01 |
| Access Restriction | Open |
| Subject Keyword | Journal: Arteriosclerosis, thrombosis, and vascular biology Endothelial Cells Vascular Endothelial Growth Factor Nuclear Receptor-77 Leukocyte Adhesion |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cardiology and Cardiovascular Medicine |
