Kitagawa N1, Inai Y, Higuchi Y, Iida H, Inai T. Inhibition of JNK in HaCaT cells induced tight junction formation with decreased expression of cytokeratin 5, cytokeratin 17 and desmoglein 3
Kitagawa N1, Inai Y, Higuchi Y, Iida H, Inai T. Inhibition of JNK in HaCaT cells induced tight junction formation with decreased expression of cytokeratin 5, cytokeratin 17 and desmoglein 3
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Kitakawa N1、Inai Y、Higuchi Y、Iida H、Inai T。HaCaT 细胞中 JNK 的抑制诱导紧密连接形成，细胞角蛋白 5、细胞角蛋白 17 和桥粒芯糖蛋白 3 的表达减少
DOI：
10.1007/s00418-014-1219-9
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发表时间：
2014
影响因子：
2.3
通讯作者：
Inai T
中科院分区：
文献类型：
--
作者：
Kitagawa N1;Inai Y;Higuchi Y;Iida H;Inai T
表皮角质形成细胞在基底层中增殖，分化，迁移通过棘层、颗粒层和皮质层，并且最终从皮肤表面剥离，分化标志物具有层特异性表达，包括细胞角蛋白和细胞-细胞连接蛋白如桥粒芯糖蛋白。基底细胞表达CK 5、CK 14和Ki 67。相反，棘层和颗粒层中的基底上细胞表达CK 1和CK 10，而不表达Ki 67。抑制人表皮角质形成细胞系HaCaT细胞中的c-Jun NH 2-末端蛋白激酶（JNK）诱导了体内颗粒层中紧密连接的形成。这些细胞失去了它们的CK 5和CK 17的表达，显示出桥粒芯糖蛋白3的表达减少，并且在核中没有Ki 67标记。这些结果表明，JNK的抑制导致HaCaT细胞从基底样和棘样细胞分化为颗粒样细胞。JNK在HaCaT细胞中的抑制为研究表皮角质形成细胞的分化提供了有用的体外模型系统。
Epidermal keratinocytes proliferate in the basal layer, differentiate, migrate through the spinous layer, granular layer and cornified layer, and finally are peeled off from the surface of skin with layer-specific expression of differentiation markers, including cytokeratins and cell–cell junction proteins such as desmogleins. Basal cells express CK5, CK14 and Ki67. In contrast, the suprabasal cells in the spinous and granular layers express CK1 and CK10 without Ki67. Inhibition of c-Jun NH2-terminal protein kinase (JNK) in HaCaT cells, a human epidermal keratinocyte cell line, induced the formation of tight junctions, which occurs in the granular layer in vivo. These cells lost their expression of CK5 and CK17, exhibited decreased expression of desmoglein 3 and had no Ki67 labeling in the nucleus. These results suggest that inhibition of JNK causes HaCaT cells to differentiate from basal- and spinous-like cells to granular-like cells. The inhibition of JNK in HaCaT cells provides a useful in vitro model system to study the differentiation of epidermal keratinocytes.