• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

[具体物质]在神经元细胞周期中对[相关基因1]、[相关基因2]和[相关基因3]基因表达调控中的可能作用:一项初步研究

Possible Role of in the Regulation of , , and Gene Expression in Neuronal Cell Cycle: A Preliminary Study.

作者信息

Bachtiar Endang W, Septiwidyati Tienneke R

机构信息

Department of Oral Biology and Oral Science Research Center, Faculty of Dentistry, Universitas Indonesia, Jakarta, Indonesia.

出版信息

J Int Soc Prev Community Dent. 2021 Sep 21;11(5):582-587. doi: 10.4103/jispcd.JISPCD_108_21. eCollection 2021 Sep-Oct.

DOI:10.4103/jispcd.JISPCD_108_21
PMID:34760804
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8533040/
Abstract

OBJECTIVE

This study aimed at evaluating the effect of exposure in gene expression of (family of transcription factors), cyclin-dependent kinase-1 (), and inducible nitric oxide synthase (iNOS) of the neuronal cell cycle.

MATERIALS AND METHODS

The culture of neuronal cell line SH-SY5Y was exposed to ATCC 33277, and the gene expression of , , and iNOS was analyzed by using a real-time polymerase chain reaction.

RESULTS

It was shown that , a G1 phase biomarker and transcription factor, was upregulated in neuronal cells exposed to compared with that in control cells. However, , a biomarker of G2/M checkpoint and iNOS, was downregulated in neuronal cells exposed to compared with that in control cells.

CONCLUSIONS

can regulate the neuronal cell cycle, as indicated in the , , and gene expression.

摘要

目的

本研究旨在评估暴露于[具体物质名称未明确,暂用“”表示]对神经元细胞周期中(转录因子家族)、细胞周期蛋白依赖性激酶-1()和诱导型一氧化氮合酶(iNOS)基因表达的影响。

材料与方法

将神经元细胞系SH-SY5Y培养物暴露于美国典型培养物保藏中心33277号菌株(此处“ATCC 33277”可能有误,推测为某种物质),并使用实时聚合酶链反应分析、和iNOS的基因表达。

结果

结果显示,作为G1期生物标志物和转录因子的,在暴露于的神经元细胞中相较于对照细胞上调。然而,作为G2/M期检查点生物标志物的和iNOS,在暴露于的神经元细胞中相较于对照细胞下调。

结论

如、和基因表达所示,可调节神经元细胞周期。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09c8/8533040/c6ab85e9f070/JISPCD-11-582-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09c8/8533040/a7b04ec5d1f6/JISPCD-11-582-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09c8/8533040/06aef4ec07ee/JISPCD-11-582-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09c8/8533040/c6ab85e9f070/JISPCD-11-582-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09c8/8533040/a7b04ec5d1f6/JISPCD-11-582-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09c8/8533040/06aef4ec07ee/JISPCD-11-582-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09c8/8533040/c6ab85e9f070/JISPCD-11-582-g003.jpg

相似文献

1
Possible Role of in the Regulation of , , and Gene Expression in Neuronal Cell Cycle: A Preliminary Study.[具体物质]在神经元细胞周期中对[相关基因1]、[相关基因2]和[相关基因3]基因表达调控中的可能作用:一项初步研究
J Int Soc Prev Community Dent. 2021 Sep 21;11(5):582-587. doi: 10.4103/jispcd.JISPCD_108_21. eCollection 2021 Sep-Oct.
2
Induction of inducible nitric oxide synthase (iNOS) in Porphyromonas gingivalis LPS-treated mouse macrophage cell line (RAW264.7) requires Toll-like receptor 9.牙龈卟啉单胞菌脂多糖处理的小鼠巨噬细胞系(RAW264.7)中诱导型一氧化氮合酶(iNOS)的诱导需要 Toll 样受体 9。
Inflamm Res. 2018 Sep;67(9):723-726. doi: 10.1007/s00011-018-1168-1. Epub 2018 Jul 6.
3
Porphyromonas gingivalis stimulates the release of nitric oxide by inducing expression of inducible nitric oxide synthases and inhibiting endothelial nitric oxide synthases.牙龈卟啉单胞菌通过诱导诱导型一氧化氮合酶的表达和抑制内皮型一氧化氮合酶的表达来刺激一氧化氮的释放。
J Periodontal Res. 2010 Jun;45(3):381-8. doi: 10.1111/j.1600-0765.2009.01249.x. Epub 2010 Mar 9.
4
Irradiation by gallium-aluminum-arsenate diode laser enhances the induction of nitric oxide by Porphyromonas gingivalis in RAW 264.7 cells.砷化镓铝二极管激光照射增强牙龈卟啉单胞菌在RAW 264.7细胞中诱导一氧化氮的生成。
J Periodontol. 2014 Sep;85(9):1259-65. doi: 10.1902/jop.2014.130744. Epub 2014 Feb 28.
5
Surface-associated material from Porphyromonas gingivalis stimulates the release of nitric oxide by inducing expression of inducible nitric oxide synthase.牙龈卟啉单胞菌的表面相关物质通过诱导诱导型一氧化氮合酶的表达来刺激一氧化氮的释放。
Microbes Infect. 2006 Feb;8(2):470-7. doi: 10.1016/j.micinf.2005.07.014. Epub 2005 Sep 19.
6
NLRP12 negatively modulates inducible nitric oxide synthase (iNOS) expression and tumor necrosis factor-α production in Porphyromonas gingivalis LPS-treated mouse macrophage cell line (RAW264.7).NLRP12 负调控牙龈卟啉单胞菌脂多糖处理的小鼠巨噬细胞系(RAW264.7)中诱导型一氧化氮合酶(iNOS)的表达和肿瘤坏死因子-α的产生。
Inflamm Res. 2019 Oct;68(10):841-844. doi: 10.1007/s00011-019-01267-3. Epub 2019 Jul 10.
7
Mice lacking inducible nitric oxide synthase demonstrate impaired killing of Porphyromonas gingivalis.缺乏诱导型一氧化氮合酶的小鼠对牙龈卟啉单胞菌的杀伤能力受损。
Infect Immun. 2003 Sep;71(9):4917-24. doi: 10.1128/IAI.71.9.4917-4924.2003.
8
Lipid A-associated proteins from Porphyromonas gingivalis stimulate release of nitric oxide by inducing expression of inducible nitric oxide synthase.牙龈卟啉单胞菌中与脂多糖A相关的蛋白质通过诱导诱导型一氧化氮合酶的表达来刺激一氧化氮的释放。
J Periodontal Res. 2007 Aug;42(4):350-60. doi: 10.1111/j.1600-0765.2006.00956.x.
9
Inducible nitric oxide synthase mediates bone development and P. gingivalis-induced alveolar bone loss.诱导型一氧化氮合酶介导骨发育及牙龈卟啉单胞菌诱导的牙槽骨丧失。
Bone. 2005 Mar;36(3):472-9. doi: 10.1016/j.bone.2004.12.002.
10
The role of E2F1-topoIIβ signaling in regulation of cell cycle exit and neuronal differentiation of human SH-SY5Y cells.E2F1-拓扑异构酶IIβ信号在调控人SH-SY5Y细胞周期退出和神经元分化中的作用。
Differentiation. 2018 Nov-Dec;104:1-12. doi: 10.1016/j.diff.2018.07.002. Epub 2018 Jul 25.

引用本文的文献

1
Periodontal Pathogens and Their Links to Neuroinflammation and Neurodegeneration.牙周病原体及其与神经炎症和神经退行性变的联系。
Microorganisms. 2023 Jul 18;11(7):1832. doi: 10.3390/microorganisms11071832.

本文引用的文献

1
Alzheimer's disease - the 'microbial hypothesis' from a clinical and neuroimaging perspective.阿尔茨海默病——从临床和神经影像学角度看“微生物假说”。
Psychiatry Res Neuroimaging. 2020 Dec 30;306:111181. doi: 10.1016/j.pscychresns.2020.111181. Epub 2020 Sep 4.
2
infection may contribute to systemic and intracerebral amyloid-beta: implications for Alzheimer's disease onset.感染可能促成全身性和脑内β-淀粉样蛋白:对阿尔茨海默病发病的影响。
Expert Rev Anti Infect Ther. 2020 Nov;18(11):1063-1066. doi: 10.1080/14787210.2020.1792292. Epub 2020 Jul 14.
3
Porphyromonas gingivalis and Alzheimer disease: Recent findings and potential therapies.
牙龈卟啉单胞菌与阿尔茨海默病:最新发现与潜在治疗策略。
J Periodontol. 2020 Oct;91 Suppl 1(Suppl 1):S45-S49. doi: 10.1002/JPER.20-0104. Epub 2020 Aug 6.
4
Context-Dependent Functions of E2F1: Cell Cycle, Cell Death, and DNA Damage Repair in Cortical Neurons.E2F1 的上下文相关功能:皮质神经元中的细胞周期、细胞死亡和 DNA 损伤修复。
Mol Neurobiol. 2020 May;57(5):2377-2390. doi: 10.1007/s12035-020-01887-5. Epub 2020 Feb 15.
5
in Alzheimer's disease brains: Evidence for disease causation and treatment with small-molecule inhibitors.在阿尔茨海默病患者大脑中:用小分子抑制剂治疗疾病的因果证据。
Sci Adv. 2019 Jan 23;5(1):eaau3333. doi: 10.1126/sciadv.aau3333. eCollection 2019 Jan.
6
Assessing the role of in periodontitis to determine a causative relationship with Alzheimer's disease.评估[具体内容缺失]在牙周炎中的作用,以确定其与阿尔茨海默病之间的因果关系。
J Oral Microbiol. 2019 Jan 29;11(1):1563405. doi: 10.1080/20002297.2018.1563405. eCollection 2019.
7
Are Outer Membrane Vesicles Microbullets for Sporadic Alzheimer's Disease Manifestation?外膜囊泡是散发性阿尔茨海默病表现的“微子弹”吗?
J Alzheimers Dis Rep. 2018 Dec 20;2(1):219-228. doi: 10.3233/ADR-180080.
8
Diosbulbin B induced G/M cell cycle arrest in hepatocytes by miRNA-186-3p and miRNA-378a-5p-mediated the decreased expression of CDK1.地榆苷 B 通过 miRNA-186-3p 和 miRNA-378a-5p 介导降低 CDK1 的表达诱导肝细胞 G/M 细胞周期停滞。
Toxicol Appl Pharmacol. 2018 Oct 15;357:1-9. doi: 10.1016/j.taap.2018.08.016. Epub 2018 Aug 23.
9
Porphyromonas gingivalis lipopolysaccharide induces cognitive dysfunction, mediated by neuronal inflammation via activation of the TLR4 signaling pathway in C57BL/6 mice.牙龈卟啉单胞菌脂多糖通过激活 TLR4 信号通路诱导 C57BL/6 小鼠神经元炎症,导致认知功能障碍。
J Neuroinflammation. 2018 Feb 9;15(1):37. doi: 10.1186/s12974-017-1052-x.
10
Role of Melt Curve Analysis in Interpretation of Nutrigenomics' MicroRNA Expression Data.熔解曲线分析在营养基因组学微小RNA表达数据解读中的作用
Cancer Genomics Proteomics. 2017 Nov-Dec;14(6):469-481. doi: 10.21873/cgp.20057.