Gene regulation and systems biology最新文献_第3页

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

Gene regulation and systems biology Pub Date : 2016-11-06 DOI: 10.4137/GRSB.S40031

J. Szostak, F. Martin, M. Talikka, M. Peitsch, J. Hoeng

{"title":"Semi-Automated Curation Allows Causal Network Model Building for the Quantification of Age-Dependent Plaque Progression in ApoE−/− Mouse","authors":"J. Szostak, F. Martin, M. Talikka, M. Peitsch, J. Hoeng","doi":"10.4137/GRSB.S40031","DOIUrl":"https://doi.org/10.4137/GRSB.S40031","url":null,"abstract":"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.","PeriodicalId":73138,"journal":{"name":"Gene regulation and systems biology","volume":"10 1","pages":"95 - 103"},"PeriodicalIF":0.0,"publicationDate":"2016-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4137/GRSB.S40031","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70702974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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

Gene regulation and systems biology 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

{"title":"Dysregulation of Protein Kinase Gene Expression in NK Cells from Chronic Fatigue Syndrome/Myalgic Encephalomyelitis Patients.","authors":"Anu Chacko, Donald R Staines, Samantha C Johnston, Sonya M Marshall-Gradisnik","doi":"10.4137/GRSB.S40036","DOIUrl":"https://doi.org/10.4137/GRSB.S40036","url":null,"abstract":"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.","PeriodicalId":73138,"journal":{"name":"Gene regulation and systems biology","volume":"10 ","pages":"85-93"},"PeriodicalIF":0.0,"publicationDate":"2016-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4137/GRSB.S40036","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34417139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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

Gene regulation and systems biology 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

{"title":"DNA Microarray Highlights Nrf2-Mediated Neuron Protection Targeted by Wasabi-Derived Isothiocyanates in IMR-32 Cells.","authors":"Phoebe Zapanta Trio, Satoru Fujisaki, Shunsuke Tanigawa, Ayami Hisanaga, Kozue Sakao, De-Xing Hou","doi":"10.4137/GRSB.S39440","DOIUrl":"https://doi.org/10.4137/GRSB.S39440","url":null,"abstract":"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. ","PeriodicalId":73138,"journal":{"name":"Gene regulation and systems biology","volume":"10 ","pages":"73-83"},"PeriodicalIF":0.0,"publicationDate":"2016-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4137/GRSB.S39440","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34324498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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

Gene regulation and systems biology 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

{"title":"Endothelial Nitric Oxide Synthase (-786T>C) and Endothelin-1 (5665G>T) Gene Polymorphisms as Vascular Dysfunction Risk Factors in Sickle Cell Anemia.","authors":"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","doi":"10.4137/GRSB.S38276","DOIUrl":"https://doi.org/10.4137/GRSB.S38276","url":null,"abstract":"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. ","PeriodicalId":73138,"journal":{"name":"Gene regulation and systems biology","volume":"10 ","pages":"67-72"},"PeriodicalIF":0.0,"publicationDate":"2016-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4137/GRSB.S38276","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34726905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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。

Gene regulation and systems biology 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

{"title":"Community-Reviewed Biological Network Models for Toxicology and Drug Discovery Applications.","authors":"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","doi":"10.4137/GRSB.S39076","DOIUrl":"10.4137/GRSB.S39076","url":null,"abstract":"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. ","PeriodicalId":73138,"journal":{"name":"Gene regulation and systems biology","volume":"10 ","pages":"51-66"},"PeriodicalIF":0.0,"publicationDate":"2016-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4944831/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34679063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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

Gene regulation and systems biology 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

{"title":"Killer Cell Immunoglobulin-like Receptor Genotype and Haplotype Investigation of Natural Killer Cells from an Australian Population of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis Patients.","authors":"T K Huth, E W Brenu, D R Staines, S M Marshall-Gradisnik","doi":"10.4137/GRSB.S39861","DOIUrl":"https://doi.org/10.4137/GRSB.S39861","url":null,"abstract":"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. ","PeriodicalId":73138,"journal":{"name":"Gene regulation and systems biology","volume":"10 ","pages":"43-9"},"PeriodicalIF":0.0,"publicationDate":"2016-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4137/GRSB.S39861","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34611684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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。

Gene regulation and systems biology Pub Date : 2016-06-16 eCollection Date: 2016-01-01 DOI: 10.4137/GRSB.S39836

Lilit Nersisyan

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。

Gene regulation and systems biology 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

{"title":"Nucleotide Interdependency in Transcription Factor Binding Sites in the Drosophila Genome.","authors":"Jacqueline M Dresch, Rowan G Zellers, Daniel K Bork, Robert A Drewell","doi":"10.4137/GRSB.S38462","DOIUrl":"10.4137/GRSB.S38462","url":null,"abstract":"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.","PeriodicalId":73138,"journal":{"name":"Gene regulation and systems biology","volume":"10 ","pages":"21-33"},"PeriodicalIF":0.0,"publicationDate":"2016-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4137/GRSB.S38462","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34599756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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。

Gene regulation and systems biology 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

{"title":"NEAT1 is Required for Survival of Breast Cancer Cells Through FUS and miR-548.","authors":"Hao Ke, Limin Zhao, Xu Feng, Haibo Xu, Li Zou, Qin Yang, Xiaosan Su, Lingtao Peng, Baowei Jiao","doi":"10.4137/GRSB.S29414","DOIUrl":"https://doi.org/10.4137/GRSB.S29414","url":null,"abstract":"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. ","PeriodicalId":73138,"journal":{"name":"Gene regulation and systems biology","volume":"10 Suppl 1","pages":"11-7"},"PeriodicalIF":0.0,"publicationDate":"2016-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4137/GRSB.S29414","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34521198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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

Gene regulation and systems biology Pub Date : 2016-01-25 DOI: 10.4137/GRSB.S35368

L. Otero, D. García, L. Wilches-Buitrago

{"title":"Expression and Presence of OPG and RANKL mRNA and Protein in Human Periodontal Ligament with Orthodontic Force","authors":"L. Otero, D. García, L. Wilches-Buitrago","doi":"10.4137/GRSB.S35368","DOIUrl":"https://doi.org/10.4137/GRSB.S35368","url":null,"abstract":"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.","PeriodicalId":73138,"journal":{"name":"Gene regulation and systems biology","volume":"10 1","pages":"15 - 20"},"PeriodicalIF":0.0,"publicationDate":"2016-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4137/GRSB.S35368","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70702957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 17