Pingyangmycin-regulated expressions of adhesion molecules in human venous malformation endothelial cells.
10.1007/s11596-012-1031-5
- Author:
Yulin JIA
1
;
Jun JIA
;
Yifang ZHAO
Author Information
1. Department of Oral and Maxillofacial Surgery, Huazhong University of Science and Technology, Wuhan, China. Jiayulin163@163.com
- Publication Type:Journal Article
- MeSH:
Bleomycin;
analogs & derivatives;
pharmacology;
Cell Adhesion Molecules;
genetics;
metabolism;
Cells, Cultured;
Endothelial Cells;
drug effects;
metabolism;
Endothelium, Vascular;
drug effects;
metabolism;
Gene Expression;
drug effects;
genetics;
Humans
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2012;32(5):760-766
- CountryChina
- Language:English
-
Abstract:
Pingyangmycin (bleomycin A5 hydrochloride, PYM) is one of the anti-neoplastic agents which have been commonly used to treat venous malformations. However, the underlying mechanism by which PYM treats venous malformations remains poorly understood. It was reported that venous endothelial cells could recruit neutrophils via adhesion molecules (E-selectin, ICAM-1, ICAM-3, VCAM-1) during the acute/chronic inflammation and subsequent histological fibrosis after sclerotherapy with PYM. This study explored if the expression of E-selectin, ICAM-1, ICAM-3 and VCAM-1 in human venous malformation endothelial cells could be affected by PYM. HVMECs were cultured from human venous malformation tissue. Expressions of E-selectin, ICAM-1, ICAM-3 and VCAM-1 on HVMECs in response to PYM were analyzed by cell ELISA. The relative levels of mRNA expression in the cells were semi-quantified. The results showed that PYM up-regulated the expressions of E-selectin, ICAM-3, VCAM-1 and ICAM-1 in both time- and concentration-dependent manner. Our findings suggested that PYM could induce the expression of adhesion molecules in HVMECs, which might be a possible mechanism by which sclerotherapy by intralesional injection of PYM treats venous malformations.
