Terminal differentiation of keratinocytes was damaged in type 2 diabetic mice.
Terminal differentiation of keratinocytes was damaged in type 2 diabetic mice.
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2 型糖尿病小鼠的角质细胞终末分化受到损害。
DOI：
10.1007/s11033-022-07367-4
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发表时间：
2022
期刊：
影响因子：
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通讯作者：
Suzuki A. Mol Biol Rep. 2022 Jul;49(7):5875-5882.
中科院分区：
文献类型：
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作者：
Takayanagi T;Hirai H;Asada Y;Yamada T;Hasegawa S;Tomatsu E;Maeda Y;Yoshino Y;Hiratsuka I;Sekiguchi-Ueda S;Shibata M;Seino Y;Sugimura Y;Akamatsu H;Itoh M;Suzuki A. Mol Biol Rep. 2022 Jul;49(7):5875-5882.
目的虽然皮肤表现在糖尿病患者中很常见，但其特征尚不清楚。本研究旨在探讨2型糖尿病(T2 DM)小鼠皮肤角质形成细胞的体内分化过程。方法取8周龄和12周龄T2 DM模型KKAy/TaJCL小鼠(KKAy)和C57BL/6JJCL小鼠(对照组)背部皮肤。用实时定量聚合酶链式反应(qRT-PCR)检测角质形成细胞分化标志物的mRNA表达。结果与对照组相比，KKAy小鼠出现高血糖。组织学结果显示KKAy小鼠表皮组织增厚，结构受损。QRT-PCR结果显示，整合素β1和角蛋白14在KKAy小鼠和对照组小鼠中的表达是一致的。然而，在KKAy小鼠中，8周时总蛋白的表达减少，12周时角蛋白10的表达减少，8周和12周时微丝蛋白和氯化蛋白的表达减少。免疫组织化学结果显示KKAy小鼠皮肤微丝蛋白表达明显减少，而Ki-67表达无明显变化。结论糖尿病小鼠皮肤终末分化过程受损，角质形成细胞增殖得以保留。角质形成细胞终末分化受损可能是糖尿病皮肤病皮肤屏障功能受损的原因之一。
AimsAlthough skin manifestations are common in diabetic patients, its characteristics are poorly identified. This study explored the differentiation process of keratinocytes in type 2 diabetes mellitus (T2DM) in vivo.MethodsBack skin of T2DM model KKAy/TaJcl mice (KKAy) and C57BL/6JJcl mice (control) aged 8 and 12 weeks was used. The mRNA expression of differentiation markers of keratinocytes was measured by quantitative real-time polymerase chain reaction (qRT-PCR). The expression of each marker in situ was examined immunohistochemically.ResultsKKAy mice showed hyperglycemia versus control mice. The histological findings showed increased thickness and structural impairment of epidermal tissue in KKAy mice. The qRT-PCR revealed that the expression of integrin beta 1 and keratin 14 in KKAy and control mice was identical. However, the expression of involucrin at 8 weeks, keratin 10 at 12 weeks, and filaggrin and loricrin at 8 and 12 weeks was decreased in KKAy mice. Immunohistochemical findings showed that filaggrin was markedly decreased in KKAy mice, though Ki-67 remained unchanged.ConclusionThe terminal differentiation process was impaired in the diabetic skin, while keratinocyte proliferation was preserved. Damaged terminal differentiation of keratinocytes may contribute to impairment of the skin barrier function in diabetic dermatoses.