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J Periodontal Res:晚期糖基化终末产物增加人口腔上皮细胞Lipocalin 2表达

2020-04-07 lishiting MedSci原创

糖尿病(DM)是牙周疾病的风险因素,能够加重牙周炎的致病状态。DM并发症的一个主要因素为晚期糖基化终末产物(AGEs),它会在牙周组织中累积并导致炎症反应。Lipocalin 2 (LCN2)是一种抗

糖尿病(DM)是牙周疾病的风险因素,能够加重牙周炎的致病状态。DM并发症的一个主要因素为晚期糖基化终末产物(AGEs),它会在牙周组织中累积并导致炎症反应。Lipocalin 2 (LCN2)是一种抗微生物肽和炎症相关因子,并且LCN2在DM中的表达水平明显增加。这篇研究的目的是为了评估AGEs和牙龈卟啉单胞菌脂多糖(P g-LPS)对人口腔上皮细胞(TR146 cells)中LCN2的影响以及LCN2分泌在牙周炎合并DM患者中所扮演的角色。

研究分别在AGEs (AGE2)和对照BSA培养条件下或添加了P g-LPS时,体外培养TR146细胞并检测细胞活性。从上皮细胞培养液中提取条件培养基并制备溶解产物,通过WB和ELISA检测LCN2, RAGE, IL-6, MAPK和NF-κB。提取AGE处理过的TR146细胞和分化的HL-60 (D-HL-60)细胞RNA,通过实时定量PCR检测LCN2和白细胞介素-6 (IL-6)的mRNAs。将RAGE-和LCN2-siRNAs (siRAGE, siLCN2)转染上皮细胞,检测AGE诱导的LCN2表达。D-HL-60细胞与TR146细胞共培养,转染siLCN2并施以AGEs刺激,检测D-HL-60细胞中IL-6 mRNA的表达以及细胞迁移情况。

结果显示,AGEs增加人上皮细胞中LCN2和IL-6的表达水平。siRAGE和RAGE中和抗体能够抑制AGE诱导的LCN2表达。AGEs促进上皮细胞中ERK, p38和NF-κB磷酸化,而它们的抑制剂会抑制AGE诱导的LCN2。相反,P g-LPS并未显著增加表达Toll-like receptor 2的TR146细胞中LCN2的表达水平。在共培养实验中,AGE诱导的LCN2抑制D-HL-60细胞中IL-6 mRNA表达,并且在上皮细胞中敲除LCN2会抑制HL-60细胞的迁移。

结论:结果表明,AGEs通过RAGE, MAPK和NF-κB信号通路增加口腔上皮细胞中 LCN2的表达,LCN2的分泌可能会影响牙周炎合并DM患者的致病状态。

原始出处:

Rie Kido, Yuka Hiroshima, et al. Advanced Glycation End-Products Increase Lipocalin 2 Expression in Human Oral Epithelial Cells. J Periodontal Res., 2020 Mar 13[Online ahead of print]

 

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    2020-06-10 feather89
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    2021-01-02 smlt2008
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    2020-04-09 lfyang
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    2020-04-09 dzx0922892
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