The late onset of necrosis and fibrosis in normal tissues can be a serious consequence of radiotherapy in cancer patients. Because radiation-induced vascular injury precedes the tissue damage, vascular injury is regarded as crucial in the pathogenesis of tissue damage. An understanding of the proces
Cyclic-strain-induced endothelial cell expression of adhesion molecules and their roles in monocyte-endothelial interaction
✍ Scribed by Yun, Jong K. ;Anderson, James M. ;Ziats, Nicholas P.
- Publisher
- John Wiley and Sons
- Year
- 1999
- Tongue
- English
- Weight
- 462 KB
- Volume
- 44
- Category
- Article
- ISSN
- 0021-9304
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✦ Synopsis
Vascular endothelial cells (ECs) are constantly subjected to hemodynamic forces that may regulate monocyte-endothelial interaction in vivo. To examine the effects of cyclic strain on endothelial expression of monocyte adhesion molecules, E-selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) ECs were exposed to physiologically relevant levels of cyclic strain. When ECs were under 25% maximal strain at 30 cycles/min for 24 h, the expression of E-selectin significantly (p < 0.05) increased, by 83%, compared to control ECs under static conditions. Similarly, monocyte adhesion to ECs under strain (maximum of 15 or 25% at 30 and 60 cycles/min for 24 h) also significantly (p < 0.05) increased, by >82%. This cyclic-strain-induced monocyte adhesion was substantially inhibited (83.5%) by anti-E-selectin antibody. ICAM-1 expres-sion also significantly increased, by 62%, when ECs were under 25% maximal strain at 30 cycles/min for 3 h whereas VCAM-1 expression by ECs under strain (for 0.5, 3, and 24 h) did not change compared to static ECs. When ECs were treated with anti-ICAM-1 antibody and monocytes with anti-VLA-4 antibody, an increase in monocyte adhesion to ECs under cyclic strain was reduced significantly. These results demonstrate that cyclic strain can induce EC expression of monocyte adhesion molecules E-selectin, ICAM-1, and VCAM-1 in a time-dependent manner and thus can mediate monocyte adhesion.
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