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实验性牙周炎诱导的低皮细胞因 IRE1α 介导的脂肪细胞内质网膜应激引起的低皮细胞

Qianqi Wu¹, Li Yan¹, Xiao Wu¹

¹Stomatology Center, Shunde Hospital, Southern Medical University, The First People's Hospital of Shunde, NO.1 Jiazi Road, Foshan, 528300, Guangdong, China.

BMC oral health

|December 22, 2023

概括

牙周炎会在内脏脂肪细胞中引发细胞内网膜压力 (ERS),从而导致缺菌性血症. 抑制IRE1α,一个关键的ERS蛋白质,有助于恢复阿迪波内克丁水平.

科学领域:

内分泌学在内分泌学.
细胞生物学细胞生物学
牙周病学牙周病学

背景情况:

低皮菌血是导致胰岛素耐药性的重要因素.
新出现的证据将牙周炎与低性菌性血症联系起来.

研究的目的:

调查牙周炎诱导的内分泌网膜应激 (ERS) 在内脏脂肪细胞中在低性菌性血症的发展中的作用.

主要方法:

已建立的小鼠牙周炎模型和通过 Porphyromonas gingivalis-lipopolysaccharide (P.g-LPS) 在体外刺激的内脏脂肪细胞.
评估了ERS标记物的蛋白质表达 (GRP78,IRE1α,PERK,ATF6) 和皮菌素.
在体内利用IRE1α抑制 (KIRA6) 和体内使用lentiviral过度表达以阐明IRE1α的作用.

主要成果:

鼠类牙周炎和P.g-LPS在体外刺激增加了ERS标志物 (GRP78,p-IRE1α/IRE1α) 和降低了内脏脂肪细胞中的亚迪波涅丁.
在牙周炎模型中抑制IRE1α部分恢复了血清阿迪波内克水平.
在接受P.g-LPS治疗的脂肪细胞中,IRE1α过度表达加剧了,而抑制恢复了阿迪波内克丁表达.

结论:

牙周炎通过内脂肪细胞的内网膜应激诱导缺菌性血症.
在牙周炎期间,IRE1α通路是内脏脂肪细胞中阿迪波涅丁表达的关键调节者.

关键词:

细胞内膜网膜应激压力在 GRP78 中使用.低皮细胞性血症 (hypoadiponectinemia) 是一个严重的疾病.这就是IRE1α.牙周病是指牙周病的发生.

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