Kim Eun Ju, Lee Dong Hun, Kim Yeon Kyung, Kim Min-Kyoung, Kim Jung Yun, Lee Min Jung, Choi Won Woo, Eun Hee Chul, Chung Jin Ho
Department of Dermatology, Seoul National University College of Medicine, Seoul, Republic of Korea; Laboratory of Cutaneous Aging Research, Biomedical Research Institute, Seoul National University Hospital, Seoul, Republic of Korea; Institute of Human-Environment Interface Biology, Seoul National University, Seoul, Republic of Korea.
Department of Dermatology, Seoul National University College of Medicine, Seoul, Republic of Korea; Laboratory of Cutaneous Aging Research, Biomedical Research Institute, Seoul National University Hospital, Seoul, Republic of Korea; Institute of Human-Environment Interface Biology, Seoul National University, Seoul, Republic of Korea.
J Dermatol Sci. 2014 Dec;76(3):214-21. doi: 10.1016/j.jdermsci.2014.09.008. Epub 2014 Oct 2.
Sensitive skin represents hyperactive sensory symptoms showing exaggerated reactions in response to internal stimulants or external irritants. Although sensitive skin is a very common condition affecting an estimated 50% of the population, its pathophysiology remains largely elusive, particularly with regard to its metabolic aspects.
The objective of our study was to investigate the pathogenesis of sensitive skin.
We recruited healthy participants with 'sensitive' or 'non-sensitive' skin based on standardized questionnaires and 10% lactic acid stinging test, and obtained skin samples for microarray analysis and subsequent experiments.
Microarray transcriptome profiling revealed that genes involved in muscle contraction, carbohydrate and lipid metabolism, and ion transport and balance were significantly decreased in sensitive skin. These altered genes could account for the abnormal muscle contraction, decreased ATP amount in sensitive skin. In addition, pain-related transcripts such as TRPV1, ASIC3 and CGRP were significantly up-regulated in sensitive skin, compared with non-sensitive skin.
Our findings suggest that sensitive skin is closely associated with the dysfunction of muscle contraction and metabolic homeostasis.
敏感性皮肤表现为感觉过敏症状,对内部刺激物或外部刺激产生过度反应。尽管敏感性皮肤是一种非常常见的状况,估计影响着50%的人群,但其病理生理学在很大程度上仍不清楚,尤其是在其代谢方面。
我们研究的目的是探究敏感性皮肤的发病机制。
我们根据标准化问卷和10%乳酸刺痛试验招募了具有“敏感”或“非敏感”皮肤的健康参与者,并获取皮肤样本用于微阵列分析及后续实验。
微阵列转录组分析显示,参与肌肉收缩、碳水化合物和脂质代谢以及离子转运和平衡的基因在敏感性皮肤中显著减少。这些改变的基因可能导致敏感性皮肤中异常的肌肉收缩、ATP含量降低。此外,与非敏感性皮肤相比,敏感性皮肤中与疼痛相关的转录本如TRPV1、ASIC3和CGRP显著上调。
我们的研究结果表明,敏感性皮肤与肌肉收缩功能障碍和代谢稳态密切相关。