Increased serum soluble vascular endothelial cadherin levels in patients with chronic spontaneous urticaria

• DOI: 10.1016/j.anai.2017.04.013
• Publication Date: 2017-06-02T21:35:13Z
• Authors: Tao Chen; Zai-pei Guo; Wen-ju Wang; Li-xin Fu; Qiao-mei Sun; Pei-mei Zhou
• Keywords: Adult; Male; 0301 basic medicine; Adolescent; Urticaria; Cell Survival; Endothelial Cells; Cadherins; Severity of Illness Index; Cell Line; Dermatitis, Atopic; 3. Good health; Young Adult; 03 medical and health sciences; Antigens, CD; Chronic Disease; Humans; Female; Phosphorylation; Child; Histamine

Chronic spontaneous urticaria (CSU) is a common skin disease characterized by recurrent itchy wheals with or without angioedema that lasts longer than 6 weeks. Vascular endothelial (VE)-cadherin is an endothelial cell-specific adhesion molecule that plays critical roles in angiogenesis and endothelial permeability.To investigate serum levels of soluble VE (sVE)-cadherin in patients with CSU.Serum levels of sVE-cadherin in patients with CSU, patients with atopic dermatitis, and healthy controls were determined by enzyme-linked immunosorbent assay. In addition, changes in sVE-cadherin serum levels were compared in patients with CSU before and after H1 antihistamine treatment. Furthermore, the effects of histamine on sVE-cadherin release by HMEC-1 cells were determined by enzyme-linked immunosorbent assay. The inhibition effects of H1 antihistamine and H2 antihistamine on sVE-cadherin release, VE-cadherin phosphorylation, and VE-cadherin disruption were evaluated in histamine-treated HMEC-1 cells by western blot and immunofluorescence.Serum levels of sVE-cadherin in patients with CSU were significantly higher than those in patients with atopic dermatitis and healthy controls. Serum sVE-cadherin levels in patients with CSU were correlated with the severity of CSU according to Urticaria Activity Scores. Furthermore, serum sVE-cadherin levels in patients with CSU at pretreatment decreased after H1 antihistamine treatment. In addition, histamine markedly induced sVE-cadherin release in HMEC-1 cells. Moreover, H1 antihistamine, but not H2 antihistamine, significantly inhibited sVE-cadherin release in histamine-treated HMEC-1 cells. Western blot data showed that histamine induced phosphorylation of VE-cadherin in HMEC-1 cells, which was blocked by H1 antihistamine.The present data showed serum levels of sVE-cadherin are increased in patients with CSU. Histamine-induced sVE-cadherin release from endothelial cells could play a role in the pathogenesis of CSU.