@article{APS4234,
author = {Hui Kang and Peng-yuan Yang and Yao-cheng Rui},
title = {Adenovirus viral interleukin-10 inhibits adhesion molecule expressions induced by hypoxia/reoxygenation in cerebrovascular endothelial cells},
journal = {Acta Pharmacologica Sinica},
volume = {29},
number = {1},
year = {2016},
keywords = {},
abstract = {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 farreaching significance in the therapy of cerebrovascular inflammatory diseases, and anti-adhesion treatment may reduce H/R injury.},
issn = {1745-7254}, url = {http://www.chinaphar.com/article/view/4234}
}