Effect of low pH on acid-sensing ion channel 1a expression in vascular endothelial cell induced by serum IgA 1 from Henoch-Sch?nlein purpura children and its mechanism
10.3969/j.issn.1001-6325.2017.12.004
- VernacularTitle:酸环境对过敏性紫癜患儿血清IgA1诱导血管内皮细胞ASIC1a表达的影响及机制
- Author:
Bo YAN
1
;
ping Li YUAN
;
di Qi PENG
;
si Gong FANG
;
jing Han DAI
Author Information
1. 安徽医学高等专科学校医学技术系
- Keywords:
Henoch-Sch?nlein purpura(HSP);
acid-sensing ion channels (ASICs);
vascular endothelium cells
- From:
Basic & Clinical Medicine
2017;37(12):1674-1680
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of low pH on acid-sensing ion channel 1a( ASIC1a) expression in vascular endothelial cells induced by serum IgA 1 from Henoch-Sch?nlein purpura ( HSP ) children and regulatory role of ASIC1a in it.Methods Human dermal microvascular endothelial cells ( HDMECs) treated by serum IgA1 from children with HSP were incubated in different pH medium .ASIC1a, destrin and α-SM mRNA expressions in HDMECs were evaluated by real-time quantitative polymerase chain reaction (q-PCR).The level of inflammatory cytokines released by vascular endothelial cells was detected by ELISA .Moreover destrin and α-SM protein expres-sion in HDMECs was evaluated by Western blot .Results The results showed that in low pH condition , IgA1 from HSP children could induce the upregulation of ASIC 1a mRNA expression , stimulate IL-8, NO and TM release of vascular endothelial cells of HSP children .And blockers of ASICs could reduce acid-induced cytokine release of vascular endothelial cells .Moreover destrin and α-SM mRNA and protein expression in HDMECs of HSP children significantly decreased when exposure to extracellular acidosis .However blockers of ASICs increased destrin and α-SM mRNA and protein expression in vascular endothelial cells of HSP children .Conclusions These findings showed that activation of ASIC 1a could be involved in the vascular endothelial cell injury of HSP children .Blocking ASIC1a may have a significant protective effect on the inflammatory injury of vascular endothelial cells .
