Abstract：
Cholinergic urticaria is a dermatological disease characterized by the presence of large patches of red skin and transient hives triggered by factors, such as exercise, sweating, and psychological tension. This skin problem is hypothesized to be attributed to a reduced expression of acetylcholinesterase (AChE), an enzyme responsible for hydrolyzing acetylcholine (ACh). Consequently, ACh is thought to the leak from sympathetic nerves to skin epidermis. The redundant ACh stimulates the mast cells to release histamine, triggering immune responses in skin. Here, the exposure of ultraviolet B in skin suppressed the expression of AChE in keratinocytes, both in in vivo and in vitro models. The decrease of the enzyme was resulted from a declined transcription of ACHE gene mediated by micro-RNAs, that is, miR-132 and miR-212. The levels of miR-132 and miR-212 were markedly induced by exposure to ultraviolet B, which subsequently suppressed the transcriptional rate of ACHE. In the presence of low level of AChE, the overflow ACh caused the pro-inflammatory responses in skin epidermis, including increased secretion of cytokines and COX-2. These findings suggest that ultraviolet B exposure is one of the factors contributing to cholinergic urticaria in skin.
摘要：
胆碱能性荨麻疹是一种皮肤病，其特征是存在大量红色皮肤和由因素引发的短暂荨麻疹，比如锻炼，出汗,和心理紧张。假设这种皮肤问题归因于乙酰胆碱酯酶（AChE）的表达减少，一种负责水解乙酰胆碱（ACh）的酶。因此,ACh被认为是从交感神经泄漏到皮肤表皮。多余的ACh刺激肥大细胞释放组胺,在皮肤中触发免疫反应。这里,皮肤中紫外线B的暴露抑制了角质形成细胞中AChE的表达，体内和体外模型。该酶的减少是由micro-RNAs介导的ACHE基因转录下降引起的，也就是说,miR-132和miR-212。暴露于紫外线B显著诱导miR-132和miR-212的水平,随后抑制了ACHE的转录率。在存在低水平的AChE的情况下，溢出ACh引起皮肤表皮的促炎反应，包括细胞因子和COX-2的分泌增加。这些发现表明，紫外线B暴露是导致皮肤胆碱能性荨麻疹的因素之一。
