Acidosis in local environment plays a critical role in cell injury. One key mediator of acidosis-induced cell injury is the acid-sensing ion channels (ASICs), particularly ASIC1a. Herein, we investigated the role of A...Acidosis in local environment plays a critical role in cell injury. One key mediator of acidosis-induced cell injury is the acid-sensing ion channels (ASICs), particularly ASIC1a. Herein, we investigated the role of ASIC1a in acid-induced vascular endothelial cell injury of Henoch-Schonlein purpura (HSP) children. Acid-induced ASIC1a, Calpain and Calcineurin expression in vascular endothelial cells pretreated with IgA1 isolated from HSP were detected by real time quantitative polymerase chain reaction and western blot methods, respectively. Cell cytotoxicity was measured by interleukin-8 and nitric oxide production with ELISA. The results showed acid-induced ASIC1a, Calpain and Calcineurin expression in cells increased, especially at PH6.5. The cytotoxicity of vascular endothelial cells was increased by extracellular acidosis. Moreover non-specific or specific blockers of ASIC1a, Amiloride and PcTX-1 could remarkably decrease these parameters. These findings show that increased [Ca<sup>2+</sup>]i, mediated via ASIC1a, might contribute to acid-induced vascular endothelial cell injury of HSP.展开更多
目的探讨MEFV基因突变与过敏性紫癜(HSP)的相关性。方法计算机检索Pub Med、Web of Science、Medline、Cochrane Library、中国期刊全文数据库(CNKI)、万方数据库,检索从建库至2015年12月31日公开发表的关于M EFV基因突变与HSP相关性的...目的探讨MEFV基因突变与过敏性紫癜(HSP)的相关性。方法计算机检索Pub Med、Web of Science、Medline、Cochrane Library、中国期刊全文数据库(CNKI)、万方数据库,检索从建库至2015年12月31日公开发表的关于M EFV基因突变与HSP相关性的文献,使用Rev Man 5.0软件进行Meta分析。结果最终纳入6篇英文文献,累计总病例数433例,其中MEFV基因突变136例,Meta分析结果显示合并的MEFV基因突变率为0.3(95%CI:0.23,0.37);3个亚组(关节炎组、消化道症状组、肾脏损害组)每组中MEFV基因突变与非突变比较均P>0.05,提示MEFV基因突变与临床症状无显著性差异。结论 MEFV基因突变可能是儿童HSP遗传易感因素,但在临床表现方面MEFV基因突变与非突变无明显的区别。展开更多
文摘Acidosis in local environment plays a critical role in cell injury. One key mediator of acidosis-induced cell injury is the acid-sensing ion channels (ASICs), particularly ASIC1a. Herein, we investigated the role of ASIC1a in acid-induced vascular endothelial cell injury of Henoch-Schonlein purpura (HSP) children. Acid-induced ASIC1a, Calpain and Calcineurin expression in vascular endothelial cells pretreated with IgA1 isolated from HSP were detected by real time quantitative polymerase chain reaction and western blot methods, respectively. Cell cytotoxicity was measured by interleukin-8 and nitric oxide production with ELISA. The results showed acid-induced ASIC1a, Calpain and Calcineurin expression in cells increased, especially at PH6.5. The cytotoxicity of vascular endothelial cells was increased by extracellular acidosis. Moreover non-specific or specific blockers of ASIC1a, Amiloride and PcTX-1 could remarkably decrease these parameters. These findings show that increased [Ca<sup>2+</sup>]i, mediated via ASIC1a, might contribute to acid-induced vascular endothelial cell injury of HSP.
文摘目的探讨MEFV基因突变与过敏性紫癜(HSP)的相关性。方法计算机检索Pub Med、Web of Science、Medline、Cochrane Library、中国期刊全文数据库(CNKI)、万方数据库,检索从建库至2015年12月31日公开发表的关于M EFV基因突变与HSP相关性的文献,使用Rev Man 5.0软件进行Meta分析。结果最终纳入6篇英文文献,累计总病例数433例,其中MEFV基因突变136例,Meta分析结果显示合并的MEFV基因突变率为0.3(95%CI:0.23,0.37);3个亚组(关节炎组、消化道症状组、肾脏损害组)每组中MEFV基因突变与非突变比较均P>0.05,提示MEFV基因突变与临床症状无显著性差异。结论 MEFV基因突变可能是儿童HSP遗传易感因素,但在临床表现方面MEFV基因突变与非突变无明显的区别。
