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SIRT1 通过调节 AP-1/饰胶蛋白聚糖信号通路介导的 PDCD4 激活来保护主动脉夹层。

SIRT1 protects against aortic dissection by regulating AP-1/decorin signaling-mediated PDCD4 activation.

机构信息

Beijing Anzhen Hospital, Beijing Aortic Disease Center, Capital Medical University, Anzhen Road 2#, Chaoyang District, Beijing, China.

出版信息

Mol Biol Rep. 2020 Mar;47(3):2149-2159. doi: 10.1007/s11033-020-05314-9. Epub 2020 Feb 18.

Abstract

Medial degeneration of aorta wall is the principal feature of aortic dissection (AD). Sirtuin 1 (SIRT1) plays essential protective effect on many aortic-associated disease. However, it is still unclear whether SIRT1participates in the process of medial degeneration-mediated AD. The purpose of this study is to explore the association between SIRT1 and AD process. qRT-PCR was used to evaluate the transcriptional level of genes involved in study. Protein levels and acetylation detection were measured by Western blotting. The regulatory relations between AP-1 and decorin was assessed by luciferase reporter gene assay. Acute aortic dissection (AAD) mice model was constructed by feeding with β-aminopropionitrile monofumarate (BAPN). Haematoxylin and eosin (HE) and Mallory staining were performed for pathological analysis. In clinical aorta tissue of thoracic aortic dissection (TAD), the expression of SIRT1, activator protein 1 (AP-1) and decorin were in accordant trend. AP-1 expression which acts on Decorin promoter region is possibly regulated in a SIRT1-mediated deacetylation dependent manner. Resveratrol or SRT1720-initiated SIRT1 activation ameliorated BAPN-induced AAD symptoms accompanied by the activation of AP-1/decorin signaling and decorin-mediated programmed cell death 4 (PDCD4) expression by inhibiting miR-21 and miR-181b. These data suggest that SIRT1/AP-1/decorin signal cascades possibly play a part role in the process of AD. Our research demonstrate that activation of SIRT1 protects against AAD symptoms by enhancing AP-1-mediated decorin expression and downstream PDCD4 signaling pathway. Possibly, SIRT1 is served as a protective factor of AD and targeting SIRT1 therapy might be an attractive therapeutic approaches for AD treatment.

摘要

主动脉壁的中层变性是主动脉夹层(AD)的主要特征。Sirtuin 1(SIRT1)对许多与主动脉相关的疾病具有重要的保护作用。然而,SIRT1 是否参与中层变性介导的 AD 过程尚不清楚。本研究旨在探讨 SIRT1 与 AD 过程的关系。qRT-PCR 用于评估参与研究的基因的转录水平。通过 Western blot 检测蛋白水平和乙酰化检测。通过荧光素酶报告基因检测评估 AP-1 和核心蛋白聚糖之间的调控关系。通过喂食β-氨基丙腈单富马酸盐(BAPN)构建急性主动脉夹层(AAD)小鼠模型。进行苏木精和伊红(HE)和马氏染色进行病理分析。在胸主动脉夹层(TAD)的临床主动脉组织中,SIRT1、激活蛋白 1(AP-1)和核心蛋白聚糖的表达呈一致趋势。可能通过 SIRT1 介导的去乙酰化依赖方式调节作用于核心蛋白聚糖启动子区域的 AP-1 表达。白藜芦醇或 SRT1720 起始的 SIRT1 激活通过抑制 miR-21 和 miR-181b 改善 BAPN 诱导的 AAD 症状,同时激活 AP-1/核心蛋白聚糖信号和核心蛋白聚糖介导的程序性细胞死亡 4(PDCD4)表达。这些数据表明,SIRT1/AP-1/核心蛋白聚糖信号级联可能在 AD 过程中发挥作用。我们的研究表明,SIRT1 的激活通过增强 AP-1 介导的核心蛋白聚糖表达和下游 PDCD4 信号通路来保护 AAD 症状。可能,SIRT1 是 AD 的保护因素,靶向 SIRT1 治疗可能是 AD 治疗的一种有吸引力的治疗方法。

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