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泛素特异性蛋白酶 5 在慢性牙周炎炎症反应中的作用。

Role of ubiquitin-specific protease 5 in the inflammatory response of chronic periodontitis.

机构信息

Department of Stomatology, Quanzhou First Hospital Affiliated to Fujian Medical University, Quanzhou, China.

出版信息

Oral Dis. 2023 Apr;29(3):1234-1241. doi: 10.1111/odi.14114. Epub 2022 Jan 16.

Abstract

BACKGROUND

The systemic inflammatory response caused by chronic periodontitis is a risk factor for multiple diseases. Ubiquitin-specific protease 5 (USP5) is a kind of deubiquitinase which mainly responsible for dissociating unanchored polyubiquitin. However, the functions of USP5 in chronic periodontitis have not been reported.

METHODS

Chronic periodontitis patients were recruited, and their periodontal samples were collected. The levels of USP5, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) in gingival crevicular fluid were evaluated by ELISA. The expression of USP5, TNF-α, IL-6, and IL-1β in human periodontal ligament stem cells (PDLSCs) was estimated by qRT-PCR assay. The activation of STAT3 signaling was examined by Western blot.

RESULTS

USP5 was upregulated in the gingival crevicular fluid and gingival tissues of chronic periodontitis patients. USP5 expression was positively correlated with the expression of proinflammatory factors. USP5 knockdown and deubiquitinase inhibitor inhibited LPS-induced inflammatory responses in PDLSCs. Suppressing USP5 inhibited STAT3 signaling in PDLSCs.

CONCLUSION

Suppression deubiquitinase USP5 inhibits the inflammatory response of chronic periodontitis by suppressing STAT3 signaling.

摘要

背景

慢性牙周炎引起的全身炎症反应是多种疾病的危险因素。泛素特异性蛋白酶 5(USP5)是一种去泛素化酶,主要负责分离未连接的多泛素。然而,USP5 在慢性牙周炎中的功能尚未报道。

方法

招募慢性牙周炎患者,并采集其牙周组织样本。通过 ELISA 评估龈沟液中 USP5、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)和白细胞介素-1β(IL-1β)的水平。通过 qRT-PCR 检测人牙周膜干细胞(PDLSCs)中 USP5、TNF-α、IL-6 和 IL-1β的表达。通过 Western blot 检测 STAT3 信号通路的激活情况。

结果

USP5 在慢性牙周炎患者的龈沟液和牙龈组织中上调。USP5 表达与促炎因子的表达呈正相关。USP5 敲低和去泛素化酶抑制剂抑制 LPS 诱导的 PDLSCs 炎症反应。抑制 USP5 抑制了 PDLSCs 中的 STAT3 信号通路。

结论

抑制去泛素化酶 USP5 通过抑制 STAT3 信号通路抑制慢性牙周炎的炎症反应。

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