This work was funded by National Natural Science Fundation of China (No 30300454 and 30271509).
Adenovirus viral interleukin-10 inhibits adhesion molecule expressions induced by hypoxia/reoxygenation in cerebrovascular endothelial cells1
Article first published online: 3 JAN 2008
Acta Pharmacologica Sinica
Volume 29, Issue 1, pages 50–56, January 2008
How to Cite
KANG, H., YANG, P.-y. and RUI, Y.-c. (2008), Adenovirus viral interleukin-10 inhibits adhesion molecule expressions induced by hypoxia/reoxygenation in cerebrovascular endothelial cells. Acta Pharmacologica Sinica, 29: 50–56. doi: 10.1111/j.1745-7254.2008.00718.x
- Issue published online: 3 JAN 2008
- Article first published online: 3 JAN 2008
- Received 2007-05-07Accepted 2007-06-23
- adhesion molecules;
- viral interleukin-10
Aim: To investigate the effects of recombinant adenovirus encoding viral interleukin-10 (vIL-10), a potent anti-inflammatory cytokine, on adhesion molecule expressions and the adhesion rates of leukocytes to endothelial cells in cerebrovascular endothelial cells injured by hypoxia/reoxygenation (H/R). Methods: A recombinant adenovirus expressing vIL-10 (Ad/vIL-10 (or the green fluorescent protein (Ad/GFP) gene was constructed. A cerebrovascular endothelial cell line bEnd.3 was pretreated with a different multiplicity of infection (MOI) of Ad/vIL-10 or Ad/GFP and then exposed to hypoxia for 9 h followed by reoxygenation for 12 h. The culture supernatants were tested for the expression of vIL-10 and endogenous murine IL-10 (mIL-10) by ELISA. The effects of Ad/vIL-10 on monocyte-endothelial cell adhesion were represented as the adhesion rate. Subsequently, the expressions of intercellular adhesion molecule 1(ICAM-1) and vascular cell adhesion molecule 1(VCAM-1) in the endothelial cells after treatment with Ad/vIL-10 and H/R were analyzed by Western blotting and real-time PCR Results: vIL-10 was expressed in cultured bEnd.3 after Ad/vIL-10 transfection and was significantly increased by H/R. Ad/vIL-10 or Ad/GFP did not affect the mIL-10 level. H/R increased the mIL-10 expression, but insignificantly. Monocyte-endothelial cell adhesion induced by H/R was significantly inhibited by pretreatment with Ad/vIL-10 (MOI: 80). ICAM-1, and VCAM-1 in bEnd.3 and were significantly increased after H/R, while pretreatment with Ad/vIL-10 (MOI: 80) significantly inhibited their expressions. Ad/GFP did not markedly affect monocyte-endothelial adhesion and the expressions of ICAM-1 and VCAM-1 induced by H/R. Conclusion: Ad/vIL-10 significantly inhibits the upregulation of endothelial adhesion molecule expressions and the increase of adhesion of monocytes-endothelial cells induced by H/R, indicating that vIL-10 gene transfer is of far-reaching significance in the therapy of cerebrovascular inflammatory diseases, and anti-adhesion treatment may reduce H/R injury.