Prostanoids induce egr1 gene expression in cementoblastic OCCM cells.
Prostanoids induce egr1 gene expression in cementoblastic OCCM cells.
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前列腺素诱导成牙骨质细胞 OCCM 细胞中的egr1基因表达。
DOI：
10.1111/j.1600-0765.2007.00972.x
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发表时间：
2007
影响因子：
3.5
通讯作者：
Tetradis,S
中科院分区：
文献类型：
--
作者：
Pham,L;Bezouglaia,O;Camargo,PM;Nervina,JM;Tetradis,S
背景和目的：激活蛋白激酶 C 信号传导的前列腺素是成牙骨质细胞 OCCM 细胞的有效合成代谢刺激剂。使用 cDNA 消减杂交，我们将早期生长反应基因-1 (egr1) 鉴定为前列腺素诱导基因。 Egr1 是一种在牙齿发育过程中表达的锌指转录因子，调节细胞生长和分化。我们假设 Egr1 可能介导成牙骨质细胞中前列腺素诱导的部分合成代谢作用。我们的目的是表征 OCCM 细胞中前列腺素诱导的 egr1 基因表达。材料和方法：通过 Northern 印迹和蛋白质免疫印迹测定来测定总 RNA 和蛋白质。结果：前列腺素 E2-、前列腺素 F2α- 和氟前列醇诱导的 egr1 mRNA 水平在 0.5 小时达到峰值，并在 4 小时时恢复到基线。与前列腺素E2相比，前列腺素F2α和氟前列醇更有效地诱导egr1。佛波醇酯（佛波醇 12-肉豆蔻酸酯 13-乙酸酯）可激活蛋白激酶 C 信号传导，诱导的egr1mRNA 水平是对照的 66 倍，而毛喉素（一种 cAMP-蛋白激酶 A 激活剂）和离子霉素（一种钙激活剂）则没有效果。蛋白激酶 C 抑制显着抑制前列腺素 E2、前列腺素 F2α 和氟前列醇诱导的egr1 mRNA 水平。最后，前列腺素在1h时最大程度地诱导Egr1蛋白。结论：egr1是前列腺素E2、前列腺素F2α和氟前列醇在OCCM细胞中通过蛋白激酶C信号传导诱导的主要反应基因，表明Egr1可能是成牙骨质细胞合成代谢反应的关键介质。牙骨质对于牙周器官的维护和再生至关重要。牙周韧带纤维（夏皮氏纤维）插入骨和牙骨质，从而支撑牙槽中的牙齿 (1)。如果牙周器官丧失，其再生需要成牙骨质细胞分化，以形成新的牙骨质以插入牙周膜纤维。事实证明，牙骨质再生的早期尝试很困难，并且很少能产生足够的组织 (2)。更好地了解促进成牙骨质细胞分化的分子和细胞调节因子对于开发有针对性的牙周再生至关重要。
Background and Objective:Prostanoids that activate protein kinase C signaling are potent anabolic stimulators of cementoblastic OCCM cells. Using cDNA subtractive hybridization, we identified early growth response gene‐1 (egr1) as a prostanoid‐induced gene. Egr1, a zinc‐finger transcription factor expressed during tooth development, regulates cell growth and differentiation. We hypothesize that Egr1 may mediate part of the prostanoid‐induced anabolic effect in cementoblasts. Our objective was to characterize prostanoid‐inducedegr1gene expression in OCCM cells.Material and Methods:Total RNA and proteins were assayed by northern blot and western immunoblot assays.Results:Prostaglandin E2‐, prostaglandin F2α‐ and fluprostenol‐inducedegr1mRNA levels peaked at 0.5 h and returned to baseline by 4 h. Prostaglandin F2α andfluprostenol more potently inducedegr1compared with prostaglandin E2. The phorbol ester, phorbol 12‐myristate 13‐acetate, which activates protein kinase C signaling, inducedegr1mRNA levels 66‐fold over the control, whereas forskolin (a cAMP‐protein kinase A activator) and ionomycin (a calcium activator) had no effect. Protein kinase C inhibition significantly inhibited prostaglandin E2‐, prostaglandin F2α‐ and fluprostenol‐inducedegr1mRNA levels. Finally, prostanoids maximally induced Egr1 protein at 1 h.Conclusion:egr1is a primary response gene induced by prostaglandin E2, prostaglandin F2αand fluprostenol in OCCM cells through protein kinase C signaling, suggesting that Egr1 may be a key mediator of anabolic responses in cementoblasts. Cementum is vital for periodontal organ maintenance and regeneration. Periodontal ligament fibers (Sharpey's fibers) insert into bone and cementum, thereby supporting the tooth in the alveolus (1). If the periodontal organ is lost, its regeneration requires cementoblast differentiation in order to form new cementum for periodontal ligament fiber insertion. Early attempts to regenerate cementum have proven difficult and rarely generate sufficient tissue (2). A better understanding of the molecular and cellular regulators that promote cementoblast differentiation is critical for developing targeted periodontal regeneration.