Biomedical Science Team, Chang Gung Institute of Technology, Taoyuan, Taiwan.
Int Endod J. 2010 Jun;43(6):461-8. doi: 10.1111/j.1365-2591.2010.01699.x.
To study prostaglandin F(2alpha) (PGF(2alpha)) receptor expression and downstream signalling in cultured human dental pulp cells and the effect of PGF(2alpha) on the alkaline phosphatase (ALP) activity of dental pulp cells.
Human dental pulp cells were cultured and exposed to PGF(2alpha). The expression of PGF(2alpha) (FP) receptors was analysed by reverse transcriptase polymerase chain reaction (RT-PCR) and Western blotting. The activation of extracellular regulated kinase (ERK) and cAMP responsive element binding protein/activating transcription factor-1 (CREB/ATF-1) signalling was determined by Western blotting. The expression of ALP in pulp cells after exposure to PGF(2alpha) was evaluated by ALP staining and PCR.
Dental pulp cells expressed FP receptor mRNA and protein. Exposure to PGF(2alpha) revealed little cytotoxicity to pulp cells. PGF(2alpha) induced both ERK and CREB/ATF-1 phosphorylation in pulp cells. Exposure to PGF(2alpha) (>1 micromol L(-1)) further decreased the ALP activity and mRNA expression. However, U0126 (an inhibitor of MEK1) showed little preventive effect on the decline of ALP activity in dental pulp cells by PGF(2alpha).
PGF(2alpha) may potentially activate FP receptors leading to ERK/CREB-ATF-1 activation during its production in inflamed dental pulp. PGF(2alpha) attenuated the ALP activity of pulp cells possibly via pathways not solely by MEK/ERK activation. PGF(2alpha) is a contributing factor of pulpal inflammation by regulating the activities of pulp cells.
研究前列腺素 F（2α）（PGF（2α））受体在培养的人牙髓细胞中的表达及其下游信号转导，以及 PGF（2α）对牙髓细胞碱性磷酸酶（ALP）活性的影响。
培养人牙髓细胞并暴露于 PGF（2α）。通过逆转录聚合酶链反应（RT-PCR）和 Western 印迹分析 PGF（2α）（FP）受体的表达。通过 Western 印迹测定细胞外调节激酶（ERK）和 cAMP 反应元件结合蛋白/激活转录因子-1（CREB/ATF-1）信号的激活。通过 ALP 染色和 PCR 评估暴露于 PGF（2α）后牙髓细胞中 ALP 的表达。
牙髓细胞表达 FP 受体 mRNA 和蛋白。暴露于 PGF（2α）对牙髓细胞几乎没有细胞毒性。PGF（2α）诱导牙髓细胞 ERK 和 CREB/ATF-1 磷酸化。暴露于 PGF（2α）（>1μmol L（-1））进一步降低了 ALP 活性和 mRNA 表达。然而，U0126（MEK1 的抑制剂）对 PGF（2α）降低牙髓细胞中 ALP 活性几乎没有预防作用。
PGF（2α）可能在炎症性牙髓中产生时通过激活 FP 受体导致 ERK/CREB-ATF-1 激活。PGF（2α）通过非 MEK/ERK 激活途径减弱牙髓细胞的 ALP 活性。PGF（2α）通过调节牙髓细胞的活性成为牙髓炎症的一个因素。
