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首页> 外文期刊>Biomaterials >Resin monomer-induced differential activation of MAP kinases and apoptosis in mouse macrophages and human pulp cells.
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Resin monomer-induced differential activation of MAP kinases and apoptosis in mouse macrophages and human pulp cells.

机译：树脂单体诱导的MAP激酶的差异激活和小鼠巨噬细胞和人类牙髓细胞的凋亡。

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摘要

Triethylene glycol dimethacrylate (TEGDMA) is a resin monomer which is released from polymerized dental composite materials. It induced apoptosis in various target cells or inhibition of LPS-induced cytokine production in cells of the immune system after prolonged exposure. In these tissues, mitogen-activated protein kinases (MAPK) regulate signal transduction pathways that support cell survival and cytokine synthesis. The time-dependent regulation of MAPK as well as their linkage to the induction of apoptosis and cytokine release under the influence of resin monomers is unknown. It was the aim of the present study to investigate the kinetics of the up- or down-regulation of the MAPK p38, JNK, and ERK1/2, the induction of apoptosis and cytokine release in RAW264.7 mouse macrophages and human pulp-derived cells. ERK1/2, p38 and JNK were differentially activated by phosphorylation in the presence of lipopolysaccharide (0.1 microg/ml; LPS), a known inducer of MAPK activity, and TEGDMA (3 mM) as detected by Western blotting. In macrophages, ERK1/2 was activated about 6-fold by LPS, while no activation was observed in the presence of TEGDMA after 15 and 30 min. A slight activation of p38 was detected in cell cultures after short exposure to TEGDMA (30 min), but activated JNK was identified after LPS stimulation only. After a long 24 h exposure period, ERK1/2 and p38 were strongly activated by LPS, a combination of LPS/TEGDMA, and TEGDMA alone (15-20-fold). In human pulp-derived cells, ERK1/2 was phosphorylated after exposure to TEGDMA up to 2 h, and sustained activation of ERK1/2 as well as p38 (12-15-fold) was detected after prolonged exposure for 24 h. The LPS-induced, time-related increase in the secretion of the pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) as well as the anti-inflammatory IL-10 was instantaneously inhibited by TEGDMA in mouse macrophages. In parallel, the percentage of cells in macrophage cultures in the stage of apoptosis and necrosis increased with exposure period. Yet, in contrast to the inhibition of cytokine release, apoptosis and necrosis caused by LPS and TEGDMA was a late response in both mouse macrophages and human pulp-derived cells. From these data it appears as if MAPK activation, inhibition of cytokine release and the induction of apoptosis and necrosis by TEGDMA are tightly related. The direct causal correlation of these phenomena, however, requires further investigation.
机译：三乙二醇二甲基丙烯酸酯（TEGDMA）是从聚合的牙科复合材料中释放出来的树脂单体。长时间暴露后，它会诱导各种靶细胞凋亡或抑制免疫系统细胞中LPS诱导的细胞因子生成。在这些组织中，促分裂原激活的蛋白激酶（MAPK）调节支持细胞存活和细胞因子合成的信号转导途径。在树脂单体的影响下，MAPK的时间依赖性调节及其与诱导凋亡和细胞因子释放的联系尚不清楚。本研究的目的是研究上调或下调MAPK p38，JNK和ERK1 / 2的动力学，诱导RAW264.7小鼠巨噬细胞和人牙髓来源的细胞凋亡和细胞因子释放的动力学。细胞。通过蛋白质印迹法检测到，在已知的MAPK活性诱导剂脂多糖（0.1 microg / ml; LPS）和磷酸化TEGDMA（3 mM）的存在下，ERK1 / 2，p38和JNK被磷酸化差异激活。在巨噬细胞中，ERP1 / 2被LPS激活了大约6倍，而在TEGDMA存在15和30分钟后未观察到激活。短时间暴露于TEGDMA（30分钟）后，在细胞培养物中检测到p38的轻度激活，但仅在LPS刺激后才能鉴定出激活的JNK。经过24小时的长时间暴露后，LPS，LPS / TEGDMA和单独的TEGDMA的组合（15-20倍）强烈激活了ERK1 / 2和p38。在人类牙髓来源的细胞中，ERK1 / 2暴露于TEGDMA长达2小时后就会被磷酸化，长时间暴露24 h后，ERK1 / 2以及p38的持续活化（12-15倍）被检测到。 LPS诱导的促炎性细胞因子肿瘤坏死因子α（TNF-alpha）和白介素6（IL-6）以及抗炎性IL-10分泌的时间相关性增加被瞬时抑制。由TEGDMA在小鼠巨噬细胞中产生。同时，在凋亡和坏死阶段巨噬细胞培养物中的细胞百分比随暴露时间的增加而增加。然而，与抑制细胞因子释放相反，LPS和TEGDMA引起的凋亡和坏死在小鼠巨噬细胞和人类牙髓来源的细胞中都是较晚的反应。从这些数据来看，似乎TEGDMA激活MAPK，抑制细胞因子释放以及诱导细胞凋亡和坏死紧密相关。但是，这些现象的直接因果关系还需要进一步研究。

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