ラット臼歯エナメル器におけるインターロイキン-6およびインターロイキン-10レセプターの免疫組織化学的局在

DOI 被引用文献1件 参考文献46件

書誌事項

タイトル別名
  • The Immunohistochemical Localization of the Interleukin-6 and Interleukin-10 Receptors during Early Odontogenesis in rat Molars

この論文をさがす

抄録

Previous studies, in which the known Jak (Janus kinase) and STAT (signal transducer and activator of transcription) isoforms were immunohistochemically mapped in developing rat molars, implied that a sizeable list of cytokine superfamily receptor (CSR) /signal-transduction pathway linkages in the cells of the enamel organ involved in the events leading directly to early amelogenesis and dentinogenesis. On the basis of the previous observations it was hypotheseized that the interleukin-6 (IL-6)receptor and the interleukin-10 (IL-10) receptor would be localized in specific sites in the cells of the enamel organ during early amelogenesis and dentinogenesis. To verify this, whole-head, freeze-dried sections were obtained from first molars of 5-day-old rats.<BR>These sections were not demineralized or fixed, reducing the possibility of false-negative results. Because the IL-6 receptor contains IL-6 receptor-α and gp 130, antibodies to the IL-6 receptor-αand gp 130, respectively, and to the IL-10 receptor, were localized using a modification of the avidinbiotincomplexmethod. TheIL-6receptor-α and gp 130 were co-localized in the pre-ameloblasts in the cervical loop, the proximal ends of pre-secretory and secretory ameloblasts, stratum intermedium, differentiating odontoblasts, odontoblasts and in the bone. The IL-10 receptor was localized in the pre -ameloblasts, the proximal ends of pre-secretory and secretory ameloblasts, stratum intermedium, differentiating odontoblasts, odontoblasts and in the bone. These findings indicate that the the IL-6 and IL-10 receptors, and their downstream signal transduction pathway linkages, are upregulated in the cells of the enamel organ and may be involved in the events leading directly to early enamel and dentin formation.

収録刊行物

被引用文献 (1)*注記

もっと見る

参考文献 (46)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ