Involvement of PI3K and PKA pathways in mouse tongue epithelial differentiation

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• 作者：Jae-Kwang Jung^a ; Hye-In Jung^b ; Sanjiv Neupane^b ; Ki-Rim Kim^c ; Ji-Youn Kim^d ; Hitoshi Yamamoto^e ; Sung-Won Cho^f ; Youngkyun Lee^b ; Hong-In Shin^g ; Wern-Joo Sohn^h ; ¹ ; ^{undine75@gmail.com} ; Jae- Young Kim^b ; ¹ ; ^{jykim91@knu.ac.kr}
• 关键词：Epithelial differentiation ; Tongue barrier formation ; Keratinization ; Multiple cell layer formation ; PI3K ; PKA
• 刊名：Acta Histochemica
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：119
• 期：1
• 页码：92-98
• 全文大小：2438 K
• 卷排序：119

文摘

In mice, tongue epithelial differentiation is mainly regulated by the interactions among various signalling molecules including Fgf signalling pathways. However, the subsequent signalling modulations for epithelial maturation, initiated by Fgf signalling, remain to be elucidated. Therefore, we employed an in vitro tongue organ cultivation system along with the applications of various pharmacological inhibitors against the intracellular signalling molecules of Fgf signalling pathways, including H89, LY294002, PD98059, and U0126. Following treatments with LY294002 and H89, inhibitors for PI3K and PKA, respectively, the decreased thickness of the tongue epithelium was observed along with the alteration in cell proliferative and apoptotic patterns. Meanwhile, cultivated tongues treated with MEK inhibitor U0126 or PD98059 showed significantly decreased cell proliferation in the tongue epithelium and the mesenchyme. Based on these results, we suggest that the tongue epithelium is differentiated into multiple epithelial cell layers via the PI3K and PKA pathways in tissue-specific manner during the epithelial-mesenchymal interactions.