Silencing ICAM-1 reduces the adhesion of vascular endothelial cells in mice with immunologic contact urticaria.

Abstract

Immunologic contact urticaria (ICU) is an immediate response of wheal caused by various contactants in vulnerable individuals, with undefined pathogenesis. In the present study, we aim to explore the effects of intercellular cell adhesion molecule-1 (ICAM-1) gene silencing by RNA inference (RNAi) on vascular endothelial cells (VECs) adhesion molecule expression and cell-cell adhesion in ICU mice. Sixty BALB/c mice were selected, among which 48 mice were used for establishment of ICU models. VECs from normal and ICU mice were grouped into different groups. Expressions of ICAM-1, eosinophilic cationic protein (ECP), total immunologlobulin E (tIgE), L-selectin (CD62L), integrin, alpha L (CD11a) in tissues and cells were evaluate by RT-qPCR and western blotting. Cell proliferation was evaluated by MTT assay and EdU staining and cell adhesive function by cell-cell adhesion assay. Compared with normal mice, ICU mice had increased expressions of ICAM-1, ECP, tIgE, CD62L, and CD11a.ICAM-1 gene silencing decreased expressions of ECP, tIgE, CD62L, and CD11a, enhanced cell proliferation, and more activity in cell adhesion. These findings indicate that RNAi-mediated gene silencing of ICAM-1 may decrease VECs adhesion expression and reduce cell-cell adhesion in mice with ICU.