期刊
JOURNAL OF INVESTIGATIVE DERMATOLOGY
卷 138, 期 6, 页码 1279-1287出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jid.2017.11.040
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资金
- Core Research for Evolutional Science and Technology of the Japan Science and Technology Agency
- Japan Society for Promotion of Science [17K07591]
- Maruho Takagi Dermatology Foundation
- Grants-in-Aid for Scientific Research [17K07591, 16H05121] Funding Source: KAKEN
The transfer of sweat to the skin surface without leakage is important for the homeostatic regulation of skin and is impaired in atopic dermatitis. Although the precise composition of the leakage barrier remains obscure, there is a large contribution from claudins, the major components of tight junctions. In humans, claudin-1, -3, and -15 are expressed on sweat ducts, and claudin-3 and -10 are expressed on secretory coils. Although only two claudins are expressed in murine sweat glands, we found that the expression of claudin-3 is conserved. Atopic dermatitis lesional skin had decreased claudin-3 expression in sweat glands, which was accompanied by sweat leakage. This critical role in water barrier function was confirmed in Cldn3(-/-) and Cldn3(+/-) mice and those with experimentally decreased claudin-3. Our results show the crucial role of claudin-3 in preventing sweat gland leakage and suggest that the pathogenesis of dermatoses accompanied by hypohidrosis involves abnormally decreased claudin-3.
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