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Semi-Automated Curation Allows Causal Network Model Building for the Quantification of Age-Dependent Plaque Progression in ApoE−/− Mouse 半自动化管理允许建立因果网络模型,用于ApoE−/−小鼠年龄依赖性斑块进展的量化
Pub Date : 2016-11-06 DOI: 10.4137/GRSB.S40031
J. Szostak, F. Martin, M. Talikka, M. Peitsch, J. Hoeng
The cellular and molecular mechanisms behind the process of atherosclerotic plaque destabilization are complex, and molecular data from aortic plaques are difficult to interpret. Biological network models may overcome these difficulties and precisely quantify the molecular mechanisms impacted during disease progression. The atherosclerosis plaque destabilization biological network model was constructed with the semiautomated curation pipeline, BELIEF. Cellular and molecular mechanisms promoting plaque destabilization or rupture were captured in the network model. Public transcriptomic data sets were used to demonstrate the specificity of the network model and to capture the different mechanisms that were impacted in ApoE−/− mouse aorta at 6 and 32 weeks. We concluded that network models combined with the network perturbation amplitude algorithm provide a sensitive, quantitative method to follow disease progression at the molecular level. This approach can be used to investigate and quantify molecular mechanisms during plaque progression.
动脉粥样硬化斑块失稳过程背后的细胞和分子机制是复杂的,主动脉斑块的分子数据很难解释。生物网络模型可以克服这些困难,并精确量化疾病进展过程中受到影响的分子机制。采用半自动管理管道BELIEF构建动脉粥样硬化斑块不稳定生物网络模型。促进斑块不稳定或破裂的细胞和分子机制在网络模型中被捕获。使用公共转录组数据集来证明网络模型的特异性,并捕获ApoE−/−小鼠主动脉在6周和32周时受到影响的不同机制。我们得出的结论是,网络模型结合网络摄动幅度算法提供了一种在分子水平上跟踪疾病进展的敏感、定量的方法。这种方法可用于研究和量化斑块进展过程中的分子机制。
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引用次数: 6
Dysregulation of Protein Kinase Gene Expression in NK Cells from Chronic Fatigue Syndrome/Myalgic Encephalomyelitis Patients. 慢性疲劳综合征/肌痛性脑脊髓炎患者NK细胞蛋白激酶基因表达失调
Pub Date : 2016-08-28 eCollection Date: 2016-01-01 DOI: 10.4137/GRSB.S40036
Anu Chacko, Donald R Staines, Samantha C Johnston, Sonya M Marshall-Gradisnik
BACKGROUND The etiology and pathomechanism of chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) are unknown. However, natural killer (NK) cell dysfunction, in particular reduced NK cytotoxic activity, is a consistent finding in CFS/ME patients. Previous research has reported significant changes in intracellular mitogen-activated protein kinase pathways from isolated NK cells. The purpose of this present investigation was to examine whether protein kinase genes have a role in abnormal NK cell intracellular signaling in CFS/ME. METHOD Messenger RNA (mRNA) expression of 528 protein kinase genes in isolated NK cells was analyzed (nCounter GX Human Kinase Kit v2 (XT); NanoString Technologies) from moderate (n = 11; age, 54.9 ± 10.3 years) and severe (n = 12; age, 47.5 ± 8.0 years) CFS/ME patients (classified by the 2011 International Consensus Criteria) and nonfatigued controls (n = 11; age, 50.0 ± 12.3 years). RESULTS The expression of 92 protein kinase genes was significantly different in the severe CFS/ME group compared with nonfatigued controls. Among these, 37 genes were significantly upregulated and 55 genes were significantly downregulated in severe CFS/ME patients compared with nonfatigued controls. CONCLUSIONS In severe CFS/ME patients, dysfunction in protein kinase genes may contribute to impairments in NK cell intracellular signaling and effector function. Similar changes in protein kinase genes may be present in other cells, potentially contributing to the pathomechanism of this illness.
背景:慢性疲劳综合征/肌痛性脑脊髓炎(CFS/ME)的病因和病理机制尚不清楚。然而,自然杀伤(NK)细胞功能障碍,特别是NK细胞毒性活性降低,在CFS/ME患者中是一致的发现。先前的研究报道了分离NK细胞的细胞内有丝分裂原激活的蛋白激酶途径的显著变化。本研究的目的是研究蛋白激酶基因是否在CFS/ME中异常NK细胞胞内信号传导中起作用。方法:采用nCounter GX Human kinase Kit v2 (XT)检测分离NK细胞中528个蛋白激酶基因的mRNA表达;NanoString Technologies) from moderate (n = 11;年龄(54.9±10.3岁)和重度(n = 12;年龄(47.5±8.0岁)CFS/ME患者(按2011年国际共识标准分类)和非疲劳对照组(n = 11;年龄:50.0±12.3岁。结果:与非疲劳对照组相比,重度CFS/ME组92个蛋白激酶基因的表达有显著差异。其中,与非疲劳对照相比,重度CFS/ME患者中有37个基因显著上调,55个基因显著下调。结论:在严重CFS/ME患者中,蛋白激酶基因功能障碍可能导致NK细胞胞内信号通路和效应物功能受损。蛋白激酶基因的类似变化可能存在于其他细胞中,可能有助于这种疾病的病理机制。
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引用次数: 11
DNA Microarray Highlights Nrf2-Mediated Neuron Protection Targeted by Wasabi-Derived Isothiocyanates in IMR-32 Cells. DNA微阵列研究发现山葵衍生异硫氰酸盐对IMR-32细胞nrf2介导的神经元保护作用
Pub Date : 2016-08-11 eCollection Date: 2016-01-01 DOI: 10.4137/GRSB.S39440
Phoebe Zapanta Trio, Satoru Fujisaki, Shunsuke Tanigawa, Ayami Hisanaga, Kozue Sakao, De-Xing Hou

6-(Methylsulfinyl)hexyl isothiocyanate (6-MSITC), 6-(methylthio)hexyl isothiocyanate (6-MTITC), and 4-(methylsulfinyl)butyl isothiocyanate (4-MSITC) are isothiocyanate (ITC) bioactive compounds from Japanese Wasabi. Previous in vivo studies highlighted the neuroprotective potential of ITCs since ITCs enhance the production of antioxidant-related enzymes. Thus, in this present study, a genome-wide DNA microarray analysis was designed to profile gene expression changes in a neuron cell line, IMR-32, stimulated by these ITCs. Among these ITCs, 6-MSITC caused the expression changes of most genes (263), of which 100 genes were upregulated and 163 genes were downregulated. Gene categorization showed that most of the differentially expressed genes are involved in oxidative stress response, and pathway analysis further revealed that Nrf2-mediated oxidative stress pathway is the top of the ITC-modulated signaling pathway. Finally, real-time polymerase chain reaction (PCR) and Western blotting confirmed the gene expression and protein products of the major targets by ITCs. Taken together, Wasabi-derived ITCs might target the Nrf2-mediated oxidative stress pathway to exert neuroprotective effects.

6-(甲基亚砜基)己基异硫氰酸酯(6- msitc)、6-(甲基亚砜基)己基异硫氰酸酯(6- mtitc)和4-(甲基亚砜基)丁基异硫氰酸酯(4- msitc)是从芥末中提取的异硫氰酸酯(ITC)生物活性化合物。先前的体内研究强调了ITCs的神经保护潜力,因为ITCs可以促进抗氧化剂相关酶的产生。因此,在本研究中,设计了全基因组DNA微阵列分析,以描述这些ITCs刺激神经元细胞系IMR-32的基因表达变化。在这些ITCs中,6-MSITC引起了大多数基因的表达变化(263个),其中100个基因表达上调,163个基因表达下调。基因分类显示大部分差异表达基因参与氧化应激反应,通路分析进一步揭示nrf2介导的氧化应激通路是itc调控的信号通路的顶端。最后通过实时聚合酶链反应(real-time polymerase chain reaction, PCR)和Western blotting对主要靶点的基因表达和蛋白产物进行验证。综上所述,芥末衍生的ITCs可能针对nrf2介导的氧化应激途径发挥神经保护作用。
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引用次数: 18
Endothelial Nitric Oxide Synthase (-786T>C) and Endothelin-1 (5665G>T) Gene Polymorphisms as Vascular Dysfunction Risk Factors in Sickle Cell Anemia. 内皮型一氧化氮合酶(-786T>C)和内皮素-1 (5665G>T)基因多态性与镰状细胞性贫血血管功能障碍的关系
Pub Date : 2016-07-28 eCollection Date: 2016-01-01 DOI: 10.4137/GRSB.S38276
Wendell Vilas-Boas, Camylla V B Figueiredo, Thassila N Pitanga, Magda O S Carvalho, Rayra P Santiago, Sânzio S Santana, Caroline C Guarda, Angela M D Zanette, Bruno A V Cerqueira, Marilda S Gonçalves

Sickle cell anemia (SCA) patients have vascular complications, and polymorphisms in endothelin-1 (ET-1) and endothelial nitric oxide synthase (eNOS) genes were associated with ET-1 and nitric oxide disturbance. We investigate the association of ET-1 5665G>T and eNOS -786T>C polymorphisms with soluble adhesion molecules (sVCAM-1 and sICAM-1), biochemical markers, and medical history. We studied 101 SCA patients; carriers of eNOS minor allele (C) had the highest levels of sVCAM-1, and carriers of ET-1 minor allele had more occurrence of acute chest syndrome (ACS). The multivariate analysis suggested the influence of the ET-1 gene on ACS outcome and an association of the eNOS gene with upper respiratory tract infection. We suggest that eNOS and ET-1 gene polymorphisms can influence SCA pathophysiology and that eNOS variant in SCA patients might be important to nitric oxide activity and vascular alteration. We found an association of the ET-1 minor allele in ACS, showing the importance of genetic screening in SCA.

镰状细胞性贫血(SCA)患者存在血管并发症,内皮素-1 (ET-1)和内皮型一氧化氮合酶(eNOS)基因多态性与ET-1和一氧化氮紊乱有关。我们研究ET-1 5665G>T和eNOS -786T>C多态性与可溶性粘附分子(sVCAM-1和sICAM-1)、生化标志物和病史的关系。我们研究了101名SCA患者;eNOS小等位基因(C)携带者sVCAM-1水平最高,ET-1小等位基因携带者急性胸综合征(ACS)发生率较高。多因素分析提示ET-1基因对ACS预后有影响,eNOS基因与上呼吸道感染有关联。我们认为eNOS和ET-1基因多态性可以影响SCA的病理生理,并且SCA患者的eNOS变异可能对一氧化氮活性和血管改变很重要。我们发现ET-1小等位基因在ACS中存在关联,表明遗传筛查在SCA中的重要性。
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引用次数: 9
Community-Reviewed Biological Network Models for Toxicology and Drug Discovery Applications. 用于毒理学和药物发现应用的社区评审生物网络模型。
Pub Date : 2016-07-12 eCollection Date: 2016-01-01 DOI: 10.4137/GRSB.S39076
Aishwarya Alex Namasivayam, Alejandro Ferreiro Morales, Ángela María Fajardo Lacave, Aravind Tallam, Borislav Simovic, David Garrido Alfaro, Dheeraj Reddy Bobbili, Florian Martin, Ganna Androsova, Irina Shvydchenko, Jennifer Park, Jorge Val Calvo, Julia Hoeng, Manuel C Peitsch, Manuel González Vélez Racero, Maria Biryukov, Marja Talikka, Modesto Berraquero Pérez, Neha Rohatgi, Noberto Díaz-Díaz, Rajesh Mandarapu, Rubén Amián Ruiz, Sergey Davidyan, Shaman Narayanasamy, Stéphanie Boué, Svetlana Guryanova, Susana Martínez Arbas, Swapna Menon, Yang Xiang

Biological network models offer a framework for understanding disease by describing the relationships between the mechanisms involved in the regulation of biological processes. Crowdsourcing can efficiently gather feedback from a wide audience with varying expertise. In the Network Verification Challenge, scientists verified and enhanced a set of 46 biological networks relevant to lung and chronic obstructive pulmonary disease. The networks were built using Biological Expression Language and contain detailed information for each node and edge, including supporting evidence from the literature. Network scoring of public transcriptomics data inferred perturbation of a subset of mechanisms and networks that matched the measured outcomes. These results, based on a computable network approach, can be used to identify novel mechanisms activated in disease, quantitatively compare different treatments and time points, and allow for assessment of data with low signal. These networks are periodically verified by the crowd to maintain an up-to-date suite of networks for toxicology and drug discovery applications.

生物网络模型通过描述生物过程调控机制之间的关系,为理解疾病提供了一个框架。众包可以有效地从具有不同专业知识的广大受众那里收集反馈。在网络验证挑战赛中,科学家们验证并增强了一组与肺部和慢性阻塞性肺病相关的 46 个生物网络。这些网络使用生物表达语言构建,包含每个节点和边缘的详细信息,包括来自文献的支持证据。对公共转录组学数据进行网络评分后,推断出与测量结果相匹配的机制和网络子集的扰动。这些结果基于可计算的网络方法,可用于识别疾病中激活的新机制,定量比较不同的治疗方法和时间点,并允许对低信号数据进行评估。这些网络会定期接受群众的验证,以维护一套最新的毒理学和药物发现应用网络。
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引用次数: 0
Killer Cell Immunoglobulin-like Receptor Genotype and Haplotype Investigation of Natural Killer Cells from an Australian Population of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis Patients. 澳大利亚慢性疲劳综合征/肌痛性脑脊髓炎患者自然杀伤细胞免疫球蛋白样受体基因型和单倍型研究
Pub Date : 2016-06-19 eCollection Date: 2016-01-01 DOI: 10.4137/GRSB.S39861
T K Huth, E W Brenu, D R Staines, S M Marshall-Gradisnik

Killer cell immunoglobulin-like receptor (KIR) genes encode for activating and inhibitory surface receptors, which are correlated with the regulation of Natural Killer (NK) cell cytotoxic activity. Reduced NK cell cytotoxic activity has been consistently reported in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) patients, and KIR haplotypes and allelic polymorphism remain to be investigated. The aim of this article was to conduct a pilot study to examine KIR genotypes, haplotypes, and allelic polymorphism in CFS/ME patients and nonfatigued controls (NFCs). Comparison of KIR and allelic polymorphism frequencies revealed no significant differences between 20 CFS/ME patients and 20 NFCs. A lower frequency of the telomeric A/B motif (P < 0.05) was observed in CFS/ME patients compared with NFCs. This pilot study is the first to report the differences in the frequency of KIR on the telomeric A/B motif in CFS/ME patients. Further studies with a larger CFS/ME cohort are required to validate these results.

杀伤细胞免疫球蛋白样受体(KIR)基因编码表面受体的激活和抑制,与自然杀伤细胞(NK)细胞毒性活性的调节有关。慢性疲劳综合征/肌痛性脑脊髓炎(CFS/ME)患者一直有NK细胞毒性活性降低的报道,KIR单倍型和等位基因多态性仍有待研究。本文的目的是开展一项初步研究,以检查CFS/ME患者和非疲劳对照(nfc)的KIR基因型、单倍型和等位基因多态性。比较20例CFS/ME患者与20例nfc患者的KIR和等位基因多态性频率无显著差异。与nfc相比,CFS/ME患者端粒A/B基序的频率较低(P < 0.05)。这项初步研究首次报道了CFS/ME患者端粒A/B基序上KIR频率的差异。需要在更大的CFS/ME队列中进行进一步的研究来验证这些结果。
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引用次数: 1
Integration of Telomere Length Dynamics into Systems Biology Framework: A Review. 端粒长度动力学整合到系统生物学框架:综述。
Pub Date : 2016-06-16 eCollection Date: 2016-01-01 DOI: 10.4137/GRSB.S39836
Lilit Nersisyan
Telomere length dynamics plays a crucial role in regulation of cellular processes and cell fate. In contrast to epidemiological studies revealing the association of telomere length with age, age-related diseases, and cancers, the role of telomeres in regulation of transcriptome and epigenome and the role of genomic variations in telomere lengthening are not extensively analyzed. This is explained by the fact that experimental assays for telomere length measurement are resource consuming, and there are very few studies where high-throughput genomics, transcriptomics, and/or epigenomics experiments have been coupled with telomere length measurements. Recent development of computational approaches for assessment of telomere length from whole genome sequencing data pave a new perspective on integration of telomeres into high-throughput systems biology analysis framework. Herein, we review existing methodologies for telomere length measurement and compare them to computational approaches, as well as discuss their applications in large-scale studies on telomere length dynamics.
端粒长度动力学在细胞过程和细胞命运的调控中起着至关重要的作用。与揭示端粒长度与年龄、年龄相关疾病和癌症相关的流行病学研究相反,端粒在调节转录组和表观基因组中的作用以及基因组变异在端粒延长中的作用尚未得到广泛分析。这是因为端粒长度测量的实验分析是消耗资源的,并且很少有高通量基因组学、转录组学和/或表观基因组学实验与端粒长度测量相结合的研究。从全基因组测序数据中评估端粒长度的计算方法的最新发展为将端粒整合到高通量系统生物学分析框架中提供了新的视角。在此,我们回顾了现有的端粒长度测量方法,并将它们与计算方法进行了比较,并讨论了它们在端粒长度动力学大规模研究中的应用。
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引用次数: 3
Nucleotide Interdependency in Transcription Factor Binding Sites in the Drosophila Genome. 果蝇基因组中转录因子结合位点的核苷酸相互依赖性。
Pub Date : 2016-06-12 eCollection Date: 2016-01-01 DOI: 10.4137/GRSB.S38462
Jacqueline M Dresch, Rowan G Zellers, Daniel K Bork, Robert A Drewell
A long-standing objective in modern biology is to characterize the molecular components that drive the development of an organism. At the heart of eukaryotic development lies gene regulation. On the molecular level, much of the research in this field has focused on the binding of transcription factors (TFs) to regulatory regions in the genome known as cis-regulatory modules (CRMs). However, relatively little is known about the sequence-specific binding preferences of many TFs, especially with respect to the possible interdependencies between the nucleotides that make up binding sites. A particular limitation of many existing algorithms that aim to predict binding site sequences is that they do not allow for dependencies between nonadjacent nucleotides. In this study, we use a recently developed computational algorithm, MARZ, to compare binding site sequences using 32 distinct models in a systematic and unbiased approach to explore nucleotide dependencies within binding sites for 15 distinct TFs known to be critical to Drosophila development. Our results indicate that many of these proteins have varying levels of nucleotide interdependencies within their DNA recognition sequences, and that, in some cases, models that account for these dependencies greatly outperform traditional models that are used to predict binding sites. We also directly compare the ability of different models to identify the known KRUPPEL TF binding sites in CRMs and demonstrate that a more complex model that accounts for nucleotide interdependencies performs better when compared with simple models. This ability to identify TFs with critical nucleotide interdependencies in their binding sites will lead to a deeper understanding of how these molecular characteristics contribute to the architecture of CRMs and the precise regulation of transcription during organismal development.
现代生物学的一个长期目标是描述驱动生物体发育的分子成分。真核生物发育的核心是基因调控。在分子水平上,该领域的大部分研究都集中在转录因子(tf)与基因组中被称为顺式调控模块(CRMs)的调控区域的结合上。然而,对许多tf的序列特异性结合偏好知之甚少,特别是关于构成结合位点的核苷酸之间可能的相互依赖性。许多旨在预测结合位点序列的现有算法的一个特殊限制是,它们不允许非相邻核苷酸之间的依赖关系。在这项研究中,我们使用最近开发的计算算法MARZ,以系统和无偏倚的方法比较32种不同模型的结合位点序列,以探索已知对果蝇发育至关重要的15种不同tf的结合位点内的核苷酸依赖性。我们的研究结果表明,许多这些蛋白质在其DNA识别序列中具有不同水平的核苷酸相互依赖性,并且,在某些情况下,考虑这些依赖性的模型大大优于用于预测结合位点的传统模型。我们还直接比较了不同模型识别crm中已知KRUPPEL TF结合位点的能力,并证明了与简单模型相比,考虑核苷酸相互依赖性的更复杂模型表现更好。这种鉴定在其结合位点上具有关键核苷酸相互依赖性的tf的能力将使我们更深入地了解这些分子特征如何促进crm的结构和在生物体发育过程中精确调节转录。
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引用次数: 3
NEAT1 is Required for Survival of Breast Cancer Cells Through FUS and miR-548. NEAT1是乳腺癌细胞通过FUS和miR-548存活所必需的。
Pub Date : 2016-04-27 eCollection Date: 2016-01-01 DOI: 10.4137/GRSB.S29414
Hao Ke, Limin Zhao, Xu Feng, Haibo Xu, Li Zou, Qin Yang, Xiaosan Su, Lingtao Peng, Baowei Jiao

Increasing evidence shows that long noncoding RNAs (lncRNAs) have important roles in the regulation of multiple cellular processes, including cell division, cell growth, and apoptosis, as well as cancer metastasis and neurological disease progression; however, the mechanism of how lncRNAs regulate these processes is not well established. In this study, we demonstrated that downregulating the expression of the lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) in breast cancer cells inhibited cell growth and induced cell apoptosis. In addition, the RNA-binding protein fused in sarcoma/translocated in liposarcoma (FUS/TLS) physically interacted with NEAT1, and reducing the expression of FUS/TLS also induced cell apoptosis. Multiple miRNAs were identified as regulators of NEAT1, but only overexpression of miR-548ar was able to decrease NEAT1 expression and promote apoptosis. These results indicate a novel interaction between NEAT1, miR-548ar-3p, and FUS and their role in the regulation of breast cancer cell apoptosis.

越来越多的证据表明,长链非编码rna (lncRNAs)在调节多种细胞过程中发挥重要作用,包括细胞分裂、细胞生长和凋亡,以及癌症转移和神经系统疾病的进展;然而,lncrna调控这些过程的机制尚不清楚。在本研究中,我们发现下调lncRNA核旁斑组装转录本1 (NEAT1)在乳腺癌细胞中的表达可抑制细胞生长并诱导细胞凋亡。此外,肉瘤中融合的rna结合蛋白/脂肉瘤易位蛋白(FUS/TLS)与NEAT1发生物理相互作用,降低FUS/TLS的表达也会诱导细胞凋亡。多种mirna被鉴定为NEAT1的调节因子,但只有过表达miR-548ar才能降低NEAT1的表达并促进细胞凋亡。这些结果表明NEAT1、miR-548ar-3p和FUS之间存在一种新的相互作用,以及它们在调节乳腺癌细胞凋亡中的作用。
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引用次数: 124
Expression and Presence of OPG and RANKL mRNA and Protein in Human Periodontal Ligament with Orthodontic Force 正畸力作用下人牙周韧带中OPG和RANKL mRNA和蛋白的表达与存在
Pub Date : 2016-01-25 DOI: 10.4137/GRSB.S35368
L. Otero, D. García, L. Wilches-Buitrago
OBJECTIVE The objective of this study is to investigate the expression and concentration of ligand receptor activator of NFkB (RANKL) and osteoprotegerin (OPG) in human periodontal ligament (hPDL) with orthodontic forces of different magnitudes. METHODS Right premolars in 32 patients were loaded with 4oz or 7oz of orthodontic force for 7 days. Left first premolars were not loaded. After 7 days, premolars were extracted for treatment as indicated. OPG and RANKL mRNA expressions were measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR), and ELISA was used to assess OPG and RANKL protein concentration in compression and tension sides of PDL. Data were subjected to analysis of variance and Tukey tests. RESULTS There was statistically significant difference in RANKL concentration on comparing control teeth with tension and compression sides of the experimental teeth (P < 0.0001). The expression of mRNA RANKL was increased in the tension and compression sides with 4oz (P < 0.0001). OPG did not show statistically significant association with any group. Changes in RANKL/OPG protein ratio in experimental and control groups showed statistically significant difference (P < 0.0001). CONCLUSIONS RANKL protein levels are elevated in hPDL loaded with orthodontic forces, suggesting that RANKL protein contributes to bone modeling in response to the initial placement of orthodontic force.
目的研究不同正畸力对人牙周韧带(hPDL)中NFkB配体受体激活因子(RANKL)和骨保护素(OPG)的表达和浓度的影响。方法对32例患者右前臼齿施加4oz或7oz的正畸力,持续7天。左第一前磨牙没有装牙。7天后,拔除前磨牙,按提示进行治疗。采用定量逆转录聚合酶链反应(qRT-PCR)检测OPG和RANKL mRNA表达,ELISA检测PDL受压侧和张力侧OPG和RANKL蛋白浓度。数据进行方差分析和Tukey检验。结果对照牙与实验牙张压侧的RANKL浓度比较,差异有统计学意义(P < 0.0001)。rrankl mRNA的表达在拉伸侧和压缩侧增加(P < 0.0001)。OPG在任何组间均无统计学意义。实验组与对照组RANKL/OPG蛋白比值变化差异有统计学意义(P < 0.0001)。结论:在加载正畸力的hPDL中,RANKL蛋白水平升高,表明RANKL蛋白在初始正畸力放置时有助于骨建模。
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引用次数: 17
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Gene regulation and systems biology
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