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海利-海利病:对可能的肌浆网钙ATP酶2上调的研究以及对分泌途径Ca2+-ATP酶1、p63和干扰素调节因子6表达的分析

Hailey-Hailey disease: investigation of a possible compensatory SERCA2 up-regulation and analysis of SPCA1, p63, and IRF6 expression.

作者信息

Zhang Dingwei, Li Xiaoli, Wang Zhenghui, Zhang Yanfei, Guo Kun, Wang Shuang, Tu Chen, Huo Jia, Xiao Shengxiang

机构信息

Department of Dermatology, The Second Affiliated Hospital of Xi'an Jiaotong University, 157 Xiwu Road, Xi'an, Shaanxi, 710004, People's Republic of China.

出版信息

Arch Dermatol Res. 2015 Mar;307(2):143-9. doi: 10.1007/s00403-014-1506-2. Epub 2014 Sep 26.

Abstract

Hailey-Hailey disease (HHD) is caused by heterozygous mutations in the ATP2C1 gene, encoding the secretory pathway Ca(2+) ATPase1 (SPCA1). SPCA1 and sarco/endoplasmic reticulum Ca(2+) ATPase2 (SERCA2) encoded by ATP2A2 are two essential calcium pumps needed for Ca(2+) homeostasis maintenance in keratinocytes. ATP2A2 mutations cause another hereditary skin disorder, Darier's disease (DD). Previously, the compensatory expression of SPCA1 for SERCA2 insufficiency in DD was demonstrated, but it is not known whether a similar compensatory mechanism exists in HHD. Additionally, little is known about the role of p63 and interferon regulatory factor 6 (IRF6), two important regulatory factors involved in keratinocyte proliferation and differentiation, in HHD. Here, we used the skin biopsy samples from patients with HHD and human primary keratinocytes transfected with ATP2C1 siRNA to search for potential pathogenic mechanisms in HHD. We observed normal SERCA2 levels, but reduced p63, and increased IRF6 levels in HHD epidermal tissues and SPCA1-deficient keratinocytes. This suggests that there is no compensatory mechanism by SERCA2 for the SPCA1 deficiency in HHD. Moreover, the abnormal expression of p63 and IRF6 appears to be related to SPCA1 haploinsufficiency, with down-regulation of p63 probably resulting from IRF6 overexpression in HHD. We speculate that a novel pathogenic mechanism involving SPCA1, p63, and IRF6 may play a role in the skin lesions occurring in HHD.

摘要

黑利-黑利病(HHD)由ATP2C1基因突变所致,该基因编码分泌途径Ca(2+)ATP酶1(SPCA1)。ATP2A2编码的SPCA1和肌浆网/内质网Ca(2+)ATP酶2(SERCA2)是维持角质形成细胞内Ca(2+)稳态所需的两种重要钙泵。ATP2A基因突变会导致另一种遗传性皮肤病——达里埃病(DD)。此前已证实DD中SPCA1可代偿SERCA2功能不足,但HHD中是否存在类似的代偿机制尚不清楚。此外,对于参与角质形成细胞增殖和分化的两个重要调节因子——p63和干扰素调节因子6(IRF6)在HHD中的作用,人们了解甚少。在此,我们利用HHD患者的皮肤活检样本以及转染了ATP2C1小干扰RNA的人原代角质形成细胞,来探寻HHD潜在致病机制。我们观察到HHD表皮组织和SPCA1缺陷型角质形成细胞中SERCA2水平正常,但p63水平降低,IRF6水平升高。这表明HHD中SERCA2不存在对SPCA1缺陷的代偿机制。此外,p63和IRF6的异常表达似乎与SPCA1单倍剂量不足有关,HHD中p63下调可能是由于IRF6过表达所致。我们推测,涉及SPCA1、p63和IRF6的一种新的致病机制可能在HHD皮肤病变中发挥作用。

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