Study of the Mechanism Underlying the Onset of Diabetic Xeroderma Focusing on an Aquaporin-3 in a Streptozotocin-Induced Diabetic Mouse Model

Ikarashi, Nobutomo; Mizukami, Nanaho; Kon, Risako; Kaneko, Miho; Uchino, Ryogo; Fujisawa, Izumi; Fukuda, Natsuko; Sakai, Hiroyasu; Kamei, Junzo

doi:10.3390/ijms20153782

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Study of the Mechanism Underlying the Onset of Diabetic Xeroderma Focusing on an Aquaporin-3 in a Streptozotocin-Induced Diabetic Mouse Model

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Department of Biomolecular Pharmacology, Hoshi University, 2-4-41 Ebara, Shinagawa-ku, Tokyo 142-8501, Japan

Authors to whom correspondence should be addressed.

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These authors contributed equally to the work.

Int. J. Mol. Sci. 2019, 20(15), 3782; https://doi.org/10.3390/ijms20153782

Received: 29 June 2019 / Revised: 30 July 2019 / Accepted: 30 July 2019 / Published: 2 August 2019

(This article belongs to the Special Issue Aquaporins: Water Channels Essential for Living Organisms 3.0)

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Abstract

Xeroderma is a frequent complication in diabetic patients. In this study, we investigated the mechanism underlying the onset of diabetic xeroderma, focusing on aquaporin-3 (AQP3), which plays an important role in water transport in the skin. Dermal water content in diabetic mice was significantly lower than that in control mice. The expression level of AQP3 in the skin was significantly lower in diabetic mice than in control mice. One week after streptozotocin (STZ) treatment, despite their increased blood glucose levels, mice showed no changes in the expression levels of AQP3, Bmal1, Clock, and D site-binding protein (Dbp) in the skin and 8-hydroxydeoxyguanosine (8-OHdG) in the urine. In contrast, two weeks after STZ treatment, mice showed increases in the blood glucose level, decreases in AQP3, Bmal1, Clock, and Dbp levels, and increases in the urinary levels of 8-OHdG. The results of this study suggest that skin AQP3 expression decreases in diabetes, which may limit water transport from the vessel side to the corneum side, causing dry skin. In addition, in diabetic mice, increased oxidative stress triggered decreases in the expression levels of Bmal1 and Clock in the skin, thereby inhibiting the transcription of Aqp3 by Dbp, which resulted in decreased AQP3 expression. View Full-Text

Keywords: aquaporin; diabetes; skin; xeroderma; streptozotocin

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Ikarashi, N.; Mizukami, N.; Kon, R.; Kaneko, M.; Uchino, R.; Fujisawa, I.; Fukuda, N.; Sakai, H.; Kamei, J. Study of the Mechanism Underlying the Onset of Diabetic Xeroderma Focusing on an Aquaporin-3 in a Streptozotocin-Induced Diabetic Mouse Model. Int. J. Mol. Sci. 2019, 20, 3782. https://doi.org/10.3390/ijms20153782

AMA Style

Ikarashi N, Mizukami N, Kon R, Kaneko M, Uchino R, Fujisawa I, Fukuda N, Sakai H, Kamei J. Study of the Mechanism Underlying the Onset of Diabetic Xeroderma Focusing on an Aquaporin-3 in a Streptozotocin-Induced Diabetic Mouse Model. International Journal of Molecular Sciences. 2019; 20(15):3782. https://doi.org/10.3390/ijms20153782

Chicago/Turabian Style

Ikarashi, Nobutomo, Nanaho Mizukami, Risako Kon, Miho Kaneko, Ryogo Uchino, Izumi Fujisawa, Natsuko Fukuda, Hiroyasu Sakai, and Junzo Kamei. 2019. "Study of the Mechanism Underlying the Onset of Diabetic Xeroderma Focusing on an Aquaporin-3 in a Streptozotocin-Induced Diabetic Mouse Model" International Journal of Molecular Sciences 20, no. 15: 3782. https://doi.org/10.3390/ijms20153782

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Study of the Mechanism Underlying the Onset of Diabetic Xeroderma Focusing on an Aquaporin-3 in a Streptozotocin-Induced Diabetic Mouse Model

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