Department of Dermatology, Second University of Naples, Italy.
Arch Dermatol Res. 2011 Sep;303(7):491-7. doi: 10.1007/s00403-011-1124-1. Epub 2011 Feb 1.
Human keratinocytes synthesize and secrete non-neuronal acetylcholine, which acts as a local cell signaling molecule, regulating functions like proliferation, cell adhesion, motility, desmosomal cell contact, and glandular activity. The keratinocyte acetylcholine axis is composed of the enzymes mediating acetylcholine synthesis (acetyltransferase) and degradation (acetylcholinesterase), and two classes of acetylcholine receptors. In this study we investigated the effect of captopril, an ACE-inhibitor, on acetylcholinesterase and acetylcholine secretion in human keratinocytes. We analyzed the level of acetylcholinesterase in HaCat and NHEK cells by RT-PCR and Western blotting analysis. In addition, the effect of captopril on AChE activity was evaluated. We found that captopril induces a strong AChE up-regulation leading to ACh degradation and reduced secretion. Our results suggest that acantholysis induced by ACE-inhibitors might be linked to altered level of Ach.
人类角质形成细胞合成并分泌非神经乙酰胆碱，作为一种局部细胞信号分子，调节增殖、细胞黏附、运动、桥粒细胞连接和腺体活性等功能。角质形成细胞乙酰胆碱轴由介导乙酰胆碱合成（乙酰转移酶）和降解（乙酰胆碱酯酶）的酶以及两类乙酰胆碱受体组成。在这项研究中，我们研究了 ACE 抑制剂卡托普利对人角质形成细胞乙酰胆碱酯酶和乙酰胆碱分泌的影响。我们通过 RT-PCR 和 Western blot 分析分析了 HaCat 和 NHEK 细胞中的乙酰胆碱酯酶水平。此外，还评估了卡托普利对 AChE 活性的影响。我们发现卡托普利诱导强烈的 AChE 上调，导致 ACh 降解和分泌减少。我们的结果表明，ACE 抑制剂诱导的棘层松解可能与 Ach 水平的改变有关。
