Role of Cutaneous Aquaporins in the Development of Xeroderma in Type 2 Diabetes

Xeroderma is induced by diabetes, reducing patients’ quality of life. We aimed to clarify the roles of cutaneous water channel aquaporin-3 (AQP3) in diabetic xeroderma using type 2 diabetes model <i>db/db</i> mice. Blood glucose levels were unchanged in 5-week-old <i>db/db</i>...

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Main Authors: Nobutomo Ikarashi, Nanaho Mizukami, Chenchen Pei, Ryogo Uchino, Izumi Fujisawa, Natsuko Fukuda, Risako Kon, Hiroyasu Sakai, Junzo Kamei
Format: Article
Language:English
Published: MDPI AG 2021-01-01
Series:Biomedicines
Subjects:
Online Access:https://www.mdpi.com/2227-9059/9/2/104
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author Nobutomo Ikarashi
Nanaho Mizukami
Chenchen Pei
Ryogo Uchino
Izumi Fujisawa
Natsuko Fukuda
Risako Kon
Hiroyasu Sakai
Junzo Kamei
author_facet Nobutomo Ikarashi
Nanaho Mizukami
Chenchen Pei
Ryogo Uchino
Izumi Fujisawa
Natsuko Fukuda
Risako Kon
Hiroyasu Sakai
Junzo Kamei
author_sort Nobutomo Ikarashi
collection DOAJ
description Xeroderma is induced by diabetes, reducing patients’ quality of life. We aimed to clarify the roles of cutaneous water channel aquaporin-3 (AQP3) in diabetic xeroderma using type 2 diabetes model <i>db/db</i> mice. Blood glucose levels were unchanged in 5-week-old <i>db/db</i> mice compared to <i>db/+</i> mice (control mice), but the pathophysiology of type 2 diabetes was confirmed in 12-week-old <i>db/db</i> mice. The dermal water content and AQP3 expression in 5-week-old <i>db/db</i> mice were almost the same as those in the control mice. On the other hand, in 12-week-old <i>db/db</i> mice, the dermal water content and AQP3 expression were significantly decreased. The addition of glucose to HaCaT cells had no effect on AQP3, but tumor necrosis factor-α (TNF-α) decreased the AQP3 expression level. Blood TNF-α levels or skin inflammation markers in the 12-week-old <i>db/db</i> mice were significantly higher than those in control mice. AQP3 levels in the skin were decreased in type 2 diabetes, and this decrease in AQP3 may be one of the causes of xeroderma. Therefore, a substance that increases AQP3 may be useful for improving xeroderma. Additionally, a decrease in skin AQP3 may be triggered by inflammation. Therefore, anti-inflammatory drugs may be effective as new therapeutic agents for diabetic xerosis.
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spelling doaj.art-3fa2008cc889431695fa1cd9bbf342ef2023-12-03T14:10:10ZengMDPI AGBiomedicines2227-90592021-01-019210410.3390/biomedicines9020104Role of Cutaneous Aquaporins in the Development of Xeroderma in Type 2 DiabetesNobutomo Ikarashi0Nanaho Mizukami1Chenchen Pei2Ryogo Uchino3Izumi Fujisawa4Natsuko Fukuda5Risako Kon6Hiroyasu Sakai7Junzo Kamei8Department of Biomolecular Pharmacology, Hoshi University, 2-4-41 Ebara, Shinagawaku, Tokyo 142-8501, JapanDepartment of Biomolecular Pharmacology, Hoshi University, 2-4-41 Ebara, Shinagawaku, Tokyo 142-8501, JapanDepartment of Biomolecular Pharmacology, Hoshi University, 2-4-41 Ebara, Shinagawaku, Tokyo 142-8501, JapanDepartment of Biomolecular Pharmacology, Hoshi University, 2-4-41 Ebara, Shinagawaku, Tokyo 142-8501, JapanDepartment of Biomolecular Pharmacology, Hoshi University, 2-4-41 Ebara, Shinagawaku, Tokyo 142-8501, JapanDepartment of Biomolecular Pharmacology, Hoshi University, 2-4-41 Ebara, Shinagawaku, Tokyo 142-8501, JapanDepartment of Biomolecular Pharmacology, Hoshi University, 2-4-41 Ebara, Shinagawaku, Tokyo 142-8501, JapanDepartment of Biomolecular Pharmacology, Hoshi University, 2-4-41 Ebara, Shinagawaku, Tokyo 142-8501, JapanDepartment of Biomolecular Pharmacology, Hoshi University, 2-4-41 Ebara, Shinagawaku, Tokyo 142-8501, JapanXeroderma is induced by diabetes, reducing patients’ quality of life. We aimed to clarify the roles of cutaneous water channel aquaporin-3 (AQP3) in diabetic xeroderma using type 2 diabetes model <i>db/db</i> mice. Blood glucose levels were unchanged in 5-week-old <i>db/db</i> mice compared to <i>db/+</i> mice (control mice), but the pathophysiology of type 2 diabetes was confirmed in 12-week-old <i>db/db</i> mice. The dermal water content and AQP3 expression in 5-week-old <i>db/db</i> mice were almost the same as those in the control mice. On the other hand, in 12-week-old <i>db/db</i> mice, the dermal water content and AQP3 expression were significantly decreased. The addition of glucose to HaCaT cells had no effect on AQP3, but tumor necrosis factor-α (TNF-α) decreased the AQP3 expression level. Blood TNF-α levels or skin inflammation markers in the 12-week-old <i>db/db</i> mice were significantly higher than those in control mice. AQP3 levels in the skin were decreased in type 2 diabetes, and this decrease in AQP3 may be one of the causes of xeroderma. Therefore, a substance that increases AQP3 may be useful for improving xeroderma. Additionally, a decrease in skin AQP3 may be triggered by inflammation. Therefore, anti-inflammatory drugs may be effective as new therapeutic agents for diabetic xerosis.https://www.mdpi.com/2227-9059/9/2/104diabetesaquaporinskinxerodermainflammationTNF-α
spellingShingle Nobutomo Ikarashi
Nanaho Mizukami
Chenchen Pei
Ryogo Uchino
Izumi Fujisawa
Natsuko Fukuda
Risako Kon
Hiroyasu Sakai
Junzo Kamei
Role of Cutaneous Aquaporins in the Development of Xeroderma in Type 2 Diabetes
Biomedicines
diabetes
aquaporin
skin
xeroderma
inflammation
TNF-α
title Role of Cutaneous Aquaporins in the Development of Xeroderma in Type 2 Diabetes
title_full Role of Cutaneous Aquaporins in the Development of Xeroderma in Type 2 Diabetes
title_fullStr Role of Cutaneous Aquaporins in the Development of Xeroderma in Type 2 Diabetes
title_full_unstemmed Role of Cutaneous Aquaporins in the Development of Xeroderma in Type 2 Diabetes
title_short Role of Cutaneous Aquaporins in the Development of Xeroderma in Type 2 Diabetes
title_sort role of cutaneous aquaporins in the development of xeroderma in type 2 diabetes
topic diabetes
aquaporin
skin
xeroderma
inflammation
TNF-α
url https://www.mdpi.com/2227-9059/9/2/104
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