Relevant bibliographies by topics / Peripheral blood mononuclear cells methylation

Academic literature on the topic 'Peripheral blood mononuclear cells methylation'

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Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Peripheral blood mononuclear cells methylation"

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Zhu, Hong, Long-Fei Wu, Xing-Bo Mo, Xin Lu, Hui Tang, Xiao-Wei Zhu, Wei Xia, et al. "Rheumatoid arthritis–associated DNA methylation sites in peripheral blood mononuclear cells." Annals of the Rheumatic Diseases 78, no. 1 (October 8, 2018): 36–42. http://dx.doi.org/10.1136/annrheumdis-2018-213970.

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ObjectivesTo identify novel DNA methylation sites significant for rheumatoid arthritis (RA) and comprehensively understand their underlying pathological mechanism.MethodsWe performed (1) genome-wide DNA methylation and mRNA expression profiling in peripheral blood mononuclear cells from RA patients and health controls; (2) correlation analysis and causal inference tests for DNA methylation and mRNA expression data; (3) differential methylation genes regulatory network construction; (4) validation tests of 10 differential methylation positions (DMPs) of interest and corresponding gene expressions; (5) correlation between PARP9 methylation and its mRNA expression level in Jurkat cells and T cells from patients with RA; (6) testing the pathological functions of PARP9 in Jurkat cells.ResultsA total of 1046 DNA methylation positions were associated with RA. The identified DMPs have regulatory effects on mRNA expressions. Causal inference tests identified six DNA methylation–mRNA–RA regulatory chains (eg, cg00959259-PARP9-RA). The identified DMPs and genes formed an interferon-inducible gene interaction network (eg, MX1, IFI44L, DTX3L and PARP9). Key DMPs and corresponding genes were validated their differences in additional samples. Methylation of PARP9 was correlated with mRNA level in Jurkat cells and T lymphocytes isolated from patients with RA. The PARP9 gene exerted significant effects on Jurkat cells (eg, cell cycle, cell proliferation, cell activation and expression of inflammatory factor IL-2).ConclusionsThis multistage study identified an interferon-inducible gene interaction network associated with RA and highlighted the importance of PARP9 gene in RA pathogenesis. The results enhanced our understanding of the important role of DNA methylation in pathology of RA.
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Zhao, M., F. Gao, X. Wu, J. Tang, and Q. Lu. "Abnormal DNA methylation in peripheral blood mononuclear cells from patients with vitiligo." British Journal of Dermatology 163, no. 4 (June 19, 2010): 736–42. http://dx.doi.org/10.1111/j.1365-2133.2010.09919.x.

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Di Francesco, Andrea, Beatrice Arosio, Anastasia Falconi, Maria Vittoria Micioni Di Bonaventura, Mohsen Karimi, Daniela Mari, Martina Casati, Mauro Maccarrone, and Claudio D’Addario. "Global changes in DNA methylation in Alzheimer’s disease peripheral blood mononuclear cells." Brain, Behavior, and Immunity 45 (March 2015): 139–44. http://dx.doi.org/10.1016/j.bbi.2014.11.002.

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Kitkumthorn, Nakarin, Time Tuangsintanakul, Prakasit Rattanatanyong, Danai Tiwawech, and Apiwat Mutirangura. "LINE-1 methylation in the peripheral blood mononuclear cells of cancer patients." Clinica Chimica Acta 413, no. 9-10 (May 2012): 869–74. http://dx.doi.org/10.1016/j.cca.2012.01.024.

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Delgado-Cruzata, Lissette, Neomi Vin-Raviv, Parisa Tehranifar, Julie Flom, Diane Reynolds, Karina Gonzalez, Regina M. Santella, and Mary Beth Terry. "Correlations in global DNA methylation measures in peripheral blood mononuclear cells and granulocytes." Epigenetics 9, no. 11 (November 2, 2014): 1504–10. http://dx.doi.org/10.4161/15592294.2014.983364.

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Tseng, Lin, Lin, Li, Yen, Chan, Tsai, et al. "Next-Generation Sequencing Profiles of the Methylome and Transcriptome in Peripheral Blood Mononuclear Cells of Rheumatoid Arthritis." Journal of Clinical Medicine 8, no. 9 (August 22, 2019): 1284. http://dx.doi.org/10.3390/jcm8091284.

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Using next-generation sequencing to decipher methylome and transcriptome and underlying molecular mechanisms contributing to rheumatoid arthritis (RA) for improving future therapies, we performed methyl-seq and RNA-seq on peripheral blood mononuclear cells (PBMCs) from RA subjects and normal donors. Principal component analysis and hierarchical clustering revealed distinct methylation signatures in RA with methylation aberrations noted across chromosomes. Methylation alterations varied with CpG features and genic characteristics. Typically, CpG islands and CpG shores were hypermethylated and displayed the greatest methylation variance. Promoters were hypermethylated and enhancers/gene bodies were hypomethylated, with methylation variance associated with expression variance. RA genetically associated genes preferentially displayed differential methylation and differential expression or interacted with differentially methylated and differentially expressed genes. These differentially methylated and differentially expressed genes were enriched with several signaling pathways and disease categories. 10 genes (CD86, RAB20, XAF1, FOLR3, LTBR, KCNH8, DOK7, PDGFA, PITPNM2, CELSR1) with concomitantly differential methylation in enhancers/promoters/gene bodies and differential expression in B cells were validated. This integrated analysis of methylome and transcriptome identified novel epigenetic signatures associated with RA and highlighted the interaction between genetics and epigenetics in RA. These findings help our understanding of the pathogenesis of RA and advance epigenetic studies in regards to the disease.
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Calabrese, Roberta, Michele Zampieri, Rosella Mechelli, Viviana Annibali, Tiziana Guastafierro, Fabio Ciccarone, Giulia Coarelli, Renato Umeton, Marco Salvetti, and Paola Caiafa. "Methylation-dependent PAD2 upregulation in multiple sclerosis peripheral blood." Multiple Sclerosis Journal 18, no. 3 (August 30, 2011): 299–304. http://dx.doi.org/10.1177/1352458511421055.

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Background: Peptidylarginine deiminase 2 (PAD2) and peptidylarginine deiminase 4 (PAD4) are two members of PAD family which are over-expressed in the multiple sclerosis (MS) brain. Through its enzymatic activity PAD2 converts myelin basic protein (MBP) arginines into citrullines – an event that may favour autoimmunity – while peptidylarginine deiminase 4 (PAD4) is involved in chromatin remodelling. Objectives: Our aim was to verify whether an altered epigenetic control of PAD2, as already shown in the MS brain, can be observed in peripheral blood mononuclear cells (PBMCs) of patients with MS since some of these cells also synthesize MBP. Methods: The expression of most suitable reference genes and of PAD2 and PAD4 was assessed by qPCR. Analysis of DNA methylation was performed by bisulfite method. Results: The comparison of PAD2 expression level in PBMCs from patients with MS vs. healthy donors showed that, as well as in the white matter of MS patients, the enzyme is significantly upregulated in affected subjects. Methylation pattern analysis of a CpG island located in the PAD2 promoter showed that over-expression is associated with promoter demethylation. Conclusion: Defective regulation of PAD2 in the periphery, without the immunological shelter of the blood–brain barrier, may contribute to the development of the autoimmune responses in MS.
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Mahurkar, S., C. Polytarchou, D. Iliopoulos, C. Pothoulakis, E. A. Mayer, and L. Chang. "Genome-wide DNA methylation profiling of peripheral blood mononuclear cells in irritable bowel syndrome." Neurogastroenterology & Motility 28, no. 3 (December 16, 2015): 410–22. http://dx.doi.org/10.1111/nmo.12741.

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Lu, Yi‐Hua, Bing‐Hua Wang, Fei Jiang, Xing‐Bo Mo, Long‐Fei Wu, Pei He, Xin Lu, Fei‐Yan Deng, and Shu‐Feng Lei. "Multi‐omics integrative analysis identified SNP‐methylation‐mRNA: Interaction in peripheral blood mononuclear cells." Journal of Cellular and Molecular Medicine 23, no. 7 (May 20, 2019): 4601–10. http://dx.doi.org/10.1111/jcmm.14315.

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Kulakova, O. G., M. R. Kabilov, L. V. Danilova, E. V. Popova, O. A. Baturina, E. Yu Tsareva, N. M. Baulina, et al. "Whole-Genome DNA Methylation Analysis of Peripheral Blood Mononuclear Cells in Multiple Sclerosis Patients with Different Disease Courses." Acta Naturae 8, no. 3 (September 15, 2016): 103–10. http://dx.doi.org/10.32607/20758251-2016-8-3-103-110.

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Multiple sclerosis (MS) is a severe neurodegenerative disease of polygenic etiology affecting the central nervous system. In addition to genetic factors, epigenetic mechanisms, primarily DNA methylation, which regulate gene expression, play an important role in MS development and progression. In this study, we have performed the first whole-genome DNA methylation profiling of peripheral blood mononuclear cells in relapsing-remitting MS (RRMS) and primary-progressive MS (PPMS) patients and compared them to those of healthy individuals in order to identify the differentially methylated CpG-sites (DMSs) associated with these common clinical disease courses. In addition, we have performed a pairwise comparison of DNA methylation profiles in RRMS and PPMS patients. All three pairwise comparisons showed significant differences in methylation profiles. Hierarchical clustering of the identified DMS methylation levels and principal component analysis for data visualization demonstrated a clearly defined aggregation of DNA samples of the compared groups into separate clusters. Compared with the control, more DMSs were identified in PPMS patients than in RRMS patients (67 and 30, respectively). More than half of DMSs are located in genes, exceeding the expected number for random distribution of DMSs between probes. RRMS patients mostly have hypomethylated DMSs, while in PPMS patients DMSs are mostly hypermethylated. CpG-islands and CpG-shores contain 60% of DMSs, identified by pairwise comparison of RRMS and control groups, and 79% of those identified by pairwise comparison of PPMS and control groups. Pairwise comparison of patients with two clinical MS courses revealed 51 DMSs, 82% of which are hypermethylated in PPMS. Overall, it was demonstrated that there are more changes in the DNA methylation profiles in PPMS than in RRMS. The data confirm the role of DNA methylation in MS development. We have shown, for the first time, that DNA methylation as an epigenetic mechanism is involved in the formation of two distinct clinical courses of MS: namely, RRMS and PPMS.
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Dissertations / Theses on the topic "Peripheral blood mononuclear cells methylation"

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Siu, Vincent. "MGMT promoter methylation and expression in glial tumours and peripheral blood mononuclear cells." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86563.

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O6-Methylguanine DNA methyltransferase (MGMT) is an inducible DNA repair protein that acts to repair damage by DNA alkylating agents currently used in chemotherapy, such as temozolomide. MGMT removes the alkyl group placed at the O6-position of guanine by these alkylating agents, decreasing their efficacy. It has been shown that epigenetic methylation of the O6-MGMT DNA promoter region in tumour tissue from glioblastoma multiforme (GBM) is associated with improved survival from patients treated with temozolomide and concomitant radiotherapy. We wanted to assess the levels of MGMT promoter methylation, RNA and protein expression of cell lines to determine if there is a correlation between these three variables. We also hypothesized that MGMT promoter methylation mosaicism exists in glial tumours and would affect response to temozolomide. To assess this mosaicism we sampled multiple regions of each tumour intra-operatively and analyzed them using methylation specific PCR. Blood was drawn from these patients and the aforementioned MGMT assays were assessed in the peripheral blood mononuclear cells (PBMCs) to determine its usefulness as a prognostic tool. Our results show that MGMT promoter methylation is not a binary event, as currently calculated, but that an intermediate levels of promoter methylation percentage can be assessed. Promoter methylation also does not correlate with RNA or protein expression, but they do trend together. MGMT promoter methylation and RNA expression also vary intratumourally. MGMT promoter methylation can also be assayed in the PBMC fraction of blood in certain patients with high grade gliomas. These methylation levels appear to be associated with recurrence of the tumour and were altered after resection. Our study shows that promoter methylation may need to be looked at as a percentage-based variable and not as a binary system. Furthermore, due to intratumoural heterogeneity more areas of a tumour may need to be assessed for promoter me
O6-Methylguanine DNA methyltransferase (MGMT) est une protéine qui répare l'ADN à la suite de dommages génétiques causées par des traitements de chimiothérapiques tel que Temozolomide (TMZ). MGMT corrige l'addition alkyle à la position O6 de guanine et par conséquence, diminue l'efficacité des agents alkylateurs. La méthylation épigénétique de la région promoteure de MGMT dans les tissues de glioblastomes corrèle avec l'augmentation de la survie des patients traités avec le TMZ et la radiothérapie. Le but de notre recherche était d'évaluer le niveau de méthylation du promoteur de MGMT, de l'ARN, et de l'expression de la protéine dans des lignées cellulaires afain de déterminer si une corrélation existe entre ces trois facteurs. De plus, nous avons prédit que le niveau de méthylation du promoteur de MGMT varierait entre chaque échantillon de tumeur cérébrale. Nous avons testé plusieurs régions d'une tumeur par (MSP). Ce teste a été performé sur les cellules périphérales mononucléaires sanguines (CPMS). Nos résultats suggèrent que le niveau de la méthylation varie énormément. De plus le niveau d'expression de l'ARN et de la protéine de MGMT ne corrèle pas avec le niveau de méthylation du promoteur de MGMT. Ces niveaux sont souvent différents chez des échantillons qui proviennent de la même tumeur. Chez certains patients diagnostiqués avec un glioblastome, le niveau de méthylation dans les CPMS semble indiquer la récidive de la tumeur. Nous suggérons que la méthylation du promoteur de MGMT n'est pas binaire, et qu'elle doit être évaluée en terme de spectre variant de zero à cent pour cent. En plus, plusieurs spécimens d'une même tumeur doit être évalué par MSP. Finallement, l'analyse des CPMS peut servir d'outil pour prédire la réponse des patients traités avec des agents alkylateurs tel que TMZ.
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Horsburgh, Steven. "An investigation into exercise-induced modifications to DNA methylation-regulatory enzymes in human peripheral blood mononuclear cells." Thesis, Northumbria University, 2016. http://nrl.northumbria.ac.uk/32545/.

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DNA methylation, an epigenetic modification which can regulate gene transcription independently from alterations to the nucleotide sequence, can be manipulated by lifestyle factors such as diet and exercise, hypothetically reversing aberrant DNA methylation associated with disease pathogenesis. The underlying mechanisms by which these changes occur are currently poorly characterised, however, in vitro data suggest that inflammatory mediators are involved. Furthermore, regular exercise appears to reduce inactivity-associated systemic inflammation, possibly by alterations to the methylome, thereby suggesting a cyclic relationship between exercise, inflammation, and epigenetic modification. The aims of this research programme, therefore, were to: characterise the acute changes that occur to the de novo DNA methyltransferases following exercise in peripheral blood mononuclear cells (PBMCs), and the role of exercise-induced systemic inflammation in this process; investigate how these changes then translate into functional modifications to the methylome; and to determine whether a training programme utilising sedentary individuals manipulates DNA methylation of genes involved in chronic systemic inflammation associated with physical inactivity. Pilot investigations corroborated previous in vitro data that recombinant IL-6 is able to regulate nuclear concentrations of DNMT3A and DNMT3B in PBMCs. In order to isolate the influence of circulating proteins independently from genetic polymorphisms that may influence susceptibility to epigenetic change, cells were stimulated with exercise-conditioned plasma following intense endurance exercise which elicited significant alterations in nuclear concentrations of DNMT3A and DNMT3B. Eccentric exercise, which is typically not associated with elevations in circulating cytokines, did not cause any significant changes in nuclear or cytoplasmic DNMT concentration, or global DNA methylation; this supports the hypothesis that transient systemic elevations in inflammatory cytokines are important regulators of epigenetic modifications associated with exercise. Lack of transcriptional changes in DNMT3A following both exercise training and an acute maximal bout suggests that, in line with in vitro data, that the observed elevations in nuclear DNMT concentration are largely due to cellular relocalisation and not gene expression of this enzyme. It remains to be elucidated whether the training regime, and the subsequent response to an acute maximal bout, is able to elicit differential methylation of IL6, NFκB2, and ASC, however, in vitro stimulation of PBMCs with the cytokines IL-6 and IL-1β did cause significant changes to IL6 promoter methylation, further supporting the role of these proteins in epigenetic regulation. The data presented in this thesis support the postulation that exercise-induced changes to DNA methylation in PBMCs likely occur due to systemic elevations of inflammatory proteins, in particular IL-6, which causes manipulation of de novo DNMT nuclear concentrations due to cellular translocation of the enzymes themselves. While it was not possible to determine whether exercise directly modified gene-specific methylation, in vitro experiments suggest that inflammatory cytokines are able to regulate IL6 promoter methylation in human PBMCs.
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LOTTO, VALENTINA. "Nutrient-gene interactions within one-carbon metabolism and effects on epigenetic regulation through dna methylation in peripheral blood mononuclear cells." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2010. http://hdl.handle.net/10281/18016.

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Epigenetics is a field of molecular biology that copes with the study of gene function regulation without variations in DNA structure or nucleotide sequences. Among the main epigenetic phenomema in eukaryotic cells there are DNA methylation and post-traslational mechanisms among which the major are histone methylation and acetylation. Epigenetic changes are potentially reversible phenomena that are controlled also by nutritional factors as the methyl-donors involved in the folate cycle. Plasma levels of B vitamins, among which “in primis” plasma folate concentrations, are implicated in epigenetic modulation so that it can be hypothesized that they may affect the modulation of gene expression through epigenetic mechanisms. Epigenetic modifications represent one of the earliest events in the genesis of some complex pathologies, therefore the study of the interaction between epigenetics and nutritional status is of great interest either to define the physiopathological mechanisms of development of some illnesses, and for possible personalized strategies of prevention. The present work has been articulated, at first, on the analysis of gene-nutritional interaction mechanisms within the folate cycle through the study of polymorphisms of enzymes involved in the metabolism of methyl-group donors; the aim was to study their possible role on the modulation of genomic DNA methylation in relationship to different plasma levels of idrosoluble B vitamins. In this regard, the most important functional polymorfisms known on the genes of one-carbon metabolism and their relationship with methylation status of polymorphonuclear cells DNA have been analyzed from a cohort of around 800 subjects within a clinical study, underlining the role of the key folate-related enzymes in the modulation of DNA methylation. Besides the function of genomic DNA methylation, the methylation status at specific sites has been also approached with the specific intent of considering a possible interrelationship between the role of promoter methylation and the co-presence of functional polymorphisms in the same genic site for a gene for which a precise functional effect is well-known. To address this issue the promoter region of coagulation factor VII gene was evaluated for both genetic and epigenetic modifications as a possible model of genetic-epigenetic interaction in the modulation of gene product regulation. The results showed the key importance of genetic-epigenetic interactions, so far unknowm, in modulating gene-expression at promoter gene sites. The role of other vitamins involved in one-carbon metabolism in major chronic diseases, and specifically the emerging role of B6 vitamin, have been also studied. Furthermore, a clinical study is now in progress to evaluate the function of gene-specific methylation in liver tissue where most of the folate cycle functions take place. The aim of this project is the evaluation of both genome-wide and gene-specific methylation status in the liver in comparison to that observed in peripheral blood mononuclear cells DNA to define whether methylation status of peripheral blood DNA may be regarded as a good systemic biomarker for this epigenetic feature of DNA in relation to B vitamins nutritional status in cancer disease. Results from this study may help to define possible functional markers of gene-nutrients interactions with effects on epigenetic modulation for future preventive or therapeutic strategies. With that purpose, a novel high-throughput array-based technique for the detection of gene-specific methylation at promoter sites has been optimized in our laboratory.
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Silva, Carolina Sousa. "Protemic characterization of peripheral blood mononuclear cells." Master's thesis, Universidade de Aveiro, 2015. http://hdl.handle.net/10773/15872.

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Mestrado em Biotecnologia - Biotecnologia Molecular
Peripheral blood mononuclear cells (PBMCs) play quite diverse and important roles in monitoring immune homeostasis. Thus, these subset of blood cells may provide access to potential physiological relevant biomolecules, namely proteins. For this reason, PBMCs represent a promising biological sample in scientific research, particularly as a source of potential biological markers discovery of the most diverse diseases. Prior studies of proteomic characterization of PBMCs from healthy individuals lack either the identification of a large number of proteins or its quantification in a way that is compatible with the search of potential biomarker candidates. Therefore, this study aimed to provide a comprehensive PBMCs proteome characterisation as well as to create a SWATH library. It was also evaluated if by using the BD Vacutainer® CPT™ tubes for PBMCs isolation, it would be possible to identify a larger number of immunologically relevant proteins in comparison to plasma samples. The enrichment test assay revealed that it is possible to identify more immune-related proteins from isolated PBMCs than from plasma. Moreover, the majority of the quantified proteins with an “immune system” GO term assigned is present in higher amounts in PBMCs samples. 2D LC-MS/MS proved to be the best approach to use in qualitative analysis of PBMCs and in the construction of a SWATH library, since it resulted in an increase of both identified and quantified proteins (66.3% and 16.9%, respectively) in comparison to 1D LC-MS/MS. A total of 2071 proteins were identified and it was possible to quantify 922 different proteins among six distinct samples. From these proteins, 445 were commom between all individuals. In conclusion, this work provides a comprehensive PBMCs proteome dataset that will be useful in further studies that focus on the search for potential biological markers of various pathologies in these cells. Additionally, SWATH-MS proved to be a reproducible and effective acquisition method to quantify PBMCs proteins.
As células mononucleares do sangue (CMS) desempenham diversos e importantes papéis na monitorização da homeostasia do sistema imunitário. Assim sendo, esta subpopulação de células sanguíneas pode providenciar acesso a potenciais biomoléculas relevantes a nível fisiológico, nomeadamente proteínas. Por esta razão, as CMS representam uma amostra biológica promissora na investigação científica, particularmente na descoberta de potenciais marcadores biológicos de diversas doenças. Estudos anteriores de caracterização proteómica das CMS de indivíduos saudáveis falharam quer na identificação de um grande número de proteínas, quer na sua quantificação, de forma compatível com a pesquisa de potenciais biomarcadores. Portanto, este estudo teve como objectivo providenciar uma caracterização proteómica abrangente, bem como a criação de uma biblioteca SWATH. Foi igualmente avaliado se usando tubos CPT™ disponíveis na BD Vacutainer® para o isolamento das CMS, seria possível identificar um maior número de proteínas imunologicamente relevantes comparativamente a amostras de plasma. O teste de enriquecimento revelou que é possível identificar mais proteínas associadas ao sistema imunitário em CMS isoladas do que em amostras de plasma. Também se verificou que a maioria das proteínas quantificadas com ontologia genética “sistema imunitário” estão presentes em maior quantidade nas amostras de CMS. 2D LC-MS/MS mostrou ser a melhor abordagem na análise qualitativa das CMS e na elaboração da biblioteca SWATH, uma vez que o número de proteínas identificadas e quantificadas apresentou um aumento de 66,3% e 16,9%, respectivamente, comparativamente à 1D LC-MS/MS. No total foram identificadas 2071 proteínas e foi possível quantificar 922 proteínas diferentes em seis amostras distintas. Destas, 445 proteínas eram comuns a todos os indivíduos. Em conclusão, este trabalho disponibiliza um amplo conjunto de dados do proteoma das CMS que será útil a estudos futuros que pretendam centrar-se na pesquisa de potenciais marcadores biológicos, nas CMS, das mais diversas patologias. Além disso, comprovou-se que o método de aquisição SWATH-MS é reprodutível e eficaz na quantificação das proteínas das CMS.
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Moser, Stephanie. "In vitro effects of psychopharmaceuticals on peripheral mononuclear blood cells." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-144429.

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Drake, Mary. "Characterisation of mononuclear cells in peripheral blood stem cell harvests." Thesis, Queen's University Belfast, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287206.

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Parkinson, Nicholas J. "Endotoxin-induced microRNA expression in equine peripheral blood mononuclear cells." Thesis, Virginia Tech, 2016. http://hdl.handle.net/10919/81766.

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The innate immune response to lipopolysaccharide (LPS) mediated by toll-like receptor 4 (TLR4) contributes substantially to the morbidity of equine gastrointestinal disease, neonatal sepsis and other diseases. MicroRNAs (miRNAs), small non-coding RNA molecules acting as post-transcriptional regulators of gene expression, have key roles in TLR4 signaling regulation in other species. The central hypothesis of this study was that LPS induces differential expression of miRNAs in equine peripheral blood mononuclear cells (PBMCs). PBMCs were isolated from healthy adult horses and cultured with LPS or medium only for 2, 4 and 8 hours. Concentrations of inflammatory cytokines were measured in supernatants by immunoassay. Illumina Next-Generation Sequencing of the miRNA transcriptome was performed in PBMCs at 0, 2 and 4 hours. Selected expression changes were verified by qRT-PCR. 327 mature miRNAs were detected in equine PBMCs. Only miR-155 was significantly upregulated by LPS. 9 miRNAs showed statistically significant expression changes with time. Tumor necrosis factor-α concentration was significantly higher in supernatants from LPS-treated cells than controls from 2 hours, while interleukin-10 and interferon-γ were increased at 8 hours. miR-155 expression was correlated to all three cytokines. These data provide a foundation for future research into miRNA involvement in equine inflammatory responses. miR-155 is the principal LPS-induced miRNA in horses. Bioinformatic target predictions support roles in regulation of innate and adaptive immune responses including TLR4 signaling, as in humans. It is thus likely to influence the acute inflammatory response to LPS. Further research will be necessary to establish its role in naturally occurring disease.
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Sibbons, Charlene. "Characterisation of polyunsaturated fatty acid synthesis in peripheral blood mononuclear cells." Thesis, University of Surrey, 2018. http://epubs.surrey.ac.uk/845807/.

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Conversion of the essential n-3 (18:3n-3) and n-6 (18:2n-6) fatty acids to longer chain polyunsaturated fatty acids (PUFA) involves sequential desaturation and elongation reactions. Previous studies have reported gender differences in n-3 PUFA synthesis, whereas the effect of age is less clear. n-3 PUFAs are reported to have important effects on immune cell function. A previous study reported long chain PUFA synthesis in mitogen stimulated but not quiescent peripheral blood mononuclear cells (PBMCs). However, the underlying mechanism is not known. PUFA synthesis was investigated in PBMCs incubated with [1-13C]18:3n-3 for 48 h. Activation with the T-lymphocyte mitogen concanavalin A (Con A) increased PUFA synthesis. 22:6n-3 synthesis was not detected. [1-13C] incorporation was greatest for 20:3n-3 suggesting initial chain elongation is an important fate for 18:3n-3. Con A increased expression of three key genes (FADS2, FADS1 and ELOVL5) involved in PUFA synthesis, suggesting upregulation of the pathway is controlled at the transcriptional level. ELOVL2 expression was negligible, possibly explaining the lack of 22:6n-3 synthesis. Con A increased methylation of 12 CpGs in the FADS2 promoter contradicting the general view that DNA methylation represses transcription. Subsequent 5’RACE analysis verified that activated PBMCs were not using an alternative promoter for FADS2 transcription. Contrary to expectation, 18:3n-3 conversion in activated PBMCs was not affected by gender or menopausal status and there was no clear age effect. PUFA synthesis was constitutive in the Jurkat T-lymphocyte leukaemic cell-line and was higher than in PBMCs. FADS2, FADS1 and ELOVL5 mRNA expression was also higher in Jurkat cells and was associated with 50% lower methylation of 17 CpGs in the FADS2 promoter, suggesting transcriptional dysregulation of PUFA synthesis in Jurkat cells involves altered DNA methylation. These findings have provided novel insights into the regulation of PUFA biosynthesis in PBMCs and upregulation of the pathway in activated PBMCs suggests that newly synthesised PUFAs may be important for cell function.
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Monteiro, Flavia Regina Goncalves. "Peripheral Blood Mononuclear Cells Cytokine Expression in Horses Treated with Dexamethasone." Thesis, Virginia Tech, 2005. http://hdl.handle.net/10919/34753.

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Glucocorticoids are widely used in horses for a variety of autoimmune and inflammatory conditions. Its potent antiinflammatory properties have been associated with the suppression of a number of different inflammatory cytokines. The purpose of the study was to evaluate the effect of dexamethasone treatment in horses on mRNA cytokine expression, including interleukin-1Î , interferon-gamma, interleukin-4 and interleukin-6, during a five day treatment period and a five day post treatment period.

A randomized complete block design was performed on 16 healthy horses. Group I (8 horses) received 0.1 mg/kg of dexamethasone sodium phosphate by intravenous injection once daily for 5 days. Group II (8 horses) received an equivalent volume of sterile saline by intravenous injection daily for 5 days. A sample of 5x10 mililiters of blood in acid citrate dextrose was obtained prior to initial treatment. Thirty minutes after each treatment injection (placebo or dexamethasone) a sample of blood was obtained during the 5 day treatment period and 24, 48, 72, 96 and 120 hours after the last treatment injection was administered. Peripheral-blood mononuclear cells were isolated from the blood samples and stimulated with concavalin A. RNA was isolated using the QIAGEN RNeasy kit. cDNA first strand synthesis was achieved using QIAGEN's OMMISCRIPT RT KIT. cDNA was also constructed for the house keeping gene Î actin. Primer pairs specific for each cytokine were designed using equine cytokine sequences available on Genbank. cDNA for each cytokine and Î -actin was amplified using Real Time PCR technique.

Interleukin-4, interleukin-6 and interferon-gamma mRNA expression was statistically significant suppressed in horses treated with dexamethasone when compared to control horses. Interleukin-1Î was only significantly suppressed on day 5. Interleukin-4, interleukin-6 and interferon-gamma mRNA expression suppression was initially observed on day 2 and lasted 24 hours after the last dose of dexamethasone was administered. Interleukin-6 mRNA expression was significantly higher when compared to control group on day 10.

Our results suggest that dexamethasone treatment of healthy horses suppresses mRNA expression of several cytokines, including interleukin-4, interleukin-6 and interferon-gamma. This effect could explain part of corticosteroid's mechanism of action for controlling inflammation in a variety of disease conditions. The time-course effect of dexamethasone showed that the effect on mRNA cytokine expression suppression is only observed on day 2 of treatment and mRNA suppression is maintained for 24 hours after discontinuation of treatment.


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Pattanaik, Malisha. "Separation of cancer cells from peripheral blood mononuclear cells using pH control and dielectrophoresis." Diss., [La Jolla] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p1469581.

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Thesis (M.S.)--University of California, San Diego, 2009.
Title from first page of PDF file (viewed October 22, 2009). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 56-59).
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Books on the topic "Peripheral blood mononuclear cells methylation"

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White, Jacquelynn Snow. Characterization of peripheral blood mononuclear cells from rabbits infected with bovine leukemia virus. 1989.

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Book chapters on the topic "Peripheral blood mononuclear cells methylation"

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Kleiveland, Charlotte R. "Peripheral Blood Mononuclear Cells." In The Impact of Food Bioactives on Health, 161–67. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-16104-4_15.

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Weinberg, Adriana. "Cryopreservation of Peripheral Blood Mononuclear Cells." In Manual of Molecular and Clinical Laboratory Immunology, 263–68. Washington, DC, USA: ASM Press, 2016. http://dx.doi.org/10.1128/9781555818722.ch27.

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Suda, Masayoshi, Ippei Shimizu, Yohko Yoshida, and Tohru Minamino. "Peripheral Blood Mononuclear Cells for Limb Ischemia." In Therapeutic Angiogenesis, 25–43. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-2744-4_3.

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Peterson, Phillip K., Burt M. Sharp, Genya Gekker, Brooks Jackson, and Henry H. Balfour. "Opiates, Human Peripheral Blood Mononuclear Cells, and HIV." In Advances in Experimental Medicine and Biology, 171–78. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5925-8_19.

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Maes, Olivier C., Howard M. Chertkow, Eugenia Wang, and Hyman M. Schipper. "Stress Gene Deregulation in Alzheimer Peripheral Blood Mononuclear Cells." In Studies on Experimental Models, 251–63. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60761-956-7_11.

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Riedhammer, Christine, Dagmar Halbritter, and Robert Weissert. "Peripheral Blood Mononuclear Cells: Isolation, Freezing, Thawing, and Culture." In Methods in Molecular Biology, 53–61. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/7651_2014_99.

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Patel, Sipahee Lal, Dinesh Kumar, Anamika Dwivedi, Payal Singh Raghuvanshi, Vishal Chand, Jaya Prakash, and Varsha Gupta. "Gene Expression Analysis from Human Peripheral Blood Mononuclear Cells." In Springer Protocols Handbooks, 193–207. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0607-0_12.

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Dispinseri, Stefania, Elisa Saba, Elisa Vicenzi, Neeltje A. Kootstra, Hanneke Schuitemaker, and Gabriella Scarlatti. "HIV-1 Isolation from Infected Peripheral Blood Mononuclear Cells." In Methods in Molecular Biology, 187–96. Totowa, NJ: Humana Press, 2014. http://dx.doi.org/10.1007/978-1-62703-670-2_15.

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Heck, Susanne, Cynthia Jane Bishop, and Richard Jonathan Ellis. "Immunophenotyping of Human Peripheral Blood Mononuclear Cells by Mass Cytometry." In Methods in Molecular Biology, 285–303. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9240-9_18.

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Melegari, Margherita, P. P. Scaglioni, C. Pasquinelli, F. Manenti, and Erica Villa. "Hepatitis B virus specific transcripts in peripheral blood mononuclear cells." In Chronically Evolving Viral Hepatitis, 46–49. Vienna: Springer Vienna, 1992. http://dx.doi.org/10.1007/978-3-7091-5633-9_10.

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Conference papers on the topic "Peripheral blood mononuclear cells methylation"

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Hyland, P. L., L. S. Burke, R. M. Pfeiffer, M. A. Tucker, A. M. Goldstein, and X. R. Yang. "Abstract A84: Reduced LINE-1 methylation in peripheral blood mononuclear cells is associated with risk of melanoma in families segregating CDKN2A germline mutations." In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Oct 22-25, 2011; Boston, MA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1940-6207.prev-11-a84.

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Rivas, A., and M. Jeffries. "SAT0490 Genome-wide DNA methylation profiling of osteoartrhitis peripheral blood mononuclear cells reveals slowed epigenetic aging among rapid radiographic progressors: data from the osteoarthritis initative (OAI)." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.6567.

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Rider, C. F., C. X. You, R. D. Edgar, S. Fan, L. M. McEwen, D. T. S. Lin, J. L. MacIsaac, et al. "Comparison of the Effects of Diesel Exhaust and Particle-Depleted Diesel Exhaust with Allergen Exposure on DNA Methylation: Bronchial Brushing and Peripheral Blood Mononuclear Cell (PBMC) Results from a Controlled Human Crossover Study." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1164.

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Yoshioka, K., T. Kawasaki, H. Sato, D. Ishii, T. Imamoto, M. Abe, Y. Hasegawa, O. Ohara, T. Suzuki, and K. Tatsumi. "Differential Transcriptome of Peripheral Mononuclear Blood Cells in Pulmonary Sarcoidosis." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3936.

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Martinakova, Z., J. Horilova, I. Lajdova, and A. Marcek Chorvatova. "Time-resolved fluorescence monitoring of cholesterol in peripheral blood mononuclear cells." In XIX Polish-Slovak-Czech Optical Conference on Wave and Quantum Aspects of Contemporary Optics, edited by Agnieszka Popiolek-Masajada and Waclaw Urbanczyk. SPIE, 2014. http://dx.doi.org/10.1117/12.2074288.

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Myerburg, MM, AS Gadgil, FC Sciurba, JM Pilewski, and SR Duncan. "Peripheral Blood Mononuclear Cells (PBMCs) from COPD Patients Mediate Airway Epithelial Injury." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1214.

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Stopinsek, Sanja, Barbara Salobir, Alojz Ihan, Saša Simčič, and Marjeta Tercelj-Zorman. "Posaconazole in vitro action on peripheral blood mononuclear cells from sarcoidosis patients." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa3268.

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Godina-Nava, J. J. "Effect of Static Magnetic Fields on the Peripheral Blood Mononuclear-like Cells." In MEDICAL PHYSICS: Sixth Mexican Symposium on Medical Physics. AIP, 2002. http://dx.doi.org/10.1063/1.1512065.

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Perniola, S., F. Cacciapaglia, D. Natuzzi, R. Bizzoca, N. Lacarpia, and F. Iannone. "AB0134 Phosphorelated stat3 expression in peripheral blood mononuclear cells in rheumatoid arthritis." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.6968.

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Ma, Shwu-Fan, Yong Huang, Rekha Vij, Steven M. Broderick, Mathew Barber, Joe G. N. Garcia, and Imre Noth. "Identification Of Idiopathic Pulmonary Fibrosis MiRNA Signature From Peripheral Blood Mononuclear Cells." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2654.

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Reports on the topic "Peripheral blood mononuclear cells methylation"

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Valeri, C. R., Linda E. Pivacek, Allan Gray, and Melissa Erban. Effects of Temperature, Length of Frozen Storage, and the Freezing Container on the Quality of Human Peripheral Blood Mononuclear Cells. Fort Belvoir, VA: Defense Technical Information Center, June 1991. http://dx.doi.org/10.21236/ada360228.

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Splitter, Gary, Zeev Trainin, and Yacov Brenner. Lymphocyte Response to Genetically Engineered Bovine Leukemia Virus Proteins in Persistently Lymphocytic Cattle from Israel and the U.S. United States Department of Agriculture, July 1995. http://dx.doi.org/10.32747/1995.7570556.bard.

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The goal of this proposal was to identify proteins of BLV recognized by lymphocyte subpopulations and determine the contribution of these proteins to viral pathogenesis. Our hypothesis was that BLV pathogenesis is governed by the T-cell response and that the immune system likely plays an important role in controlling the utcome of infection. Our studies presented in ths final report demonstrate that T cell competency declines with advancing stages of infection. Dramatic differences were observed in lymphocyte proliferation to recombinant proteins encoded by BLV gag (p12, p15, and p24) and env (gp30 and gp15) genes in different disease stages. Because retroviruses are known to mutate frequently, examinatin of infected cattle from both Israel and the United States will likely detect variability in the immune response. This combined research approach provides the first opportunity to selectively address the importance of T-cell proliferation to BLV proteins and cytokines produced during different stages of BLV infection. Lack of this information regarding BLV infection has hindered understanding lympocyte regulation of BLV pathogenesis. We have developed the essential reagents necessary to determine the prominence of different lymphocyte subpopulations and cytokines produced during the different disease stages within the natural host. We found that type 1 cytokines (IL-2 and IFN-g) increased in PBMCs from animals in early disease, and decreasd in PBMCs from animals in late disease stages of BLV infection, while IL-10, increased with disease progression. Recently, a dichotomy between IL-12 and IL-10 has emerged in regards to progression of a variety of diseases. IL-12 activates type 1 cytokine production and has an antagonistic effect on type 2 cytokines. Here, using quantitative competitive PCR, we show that peripheral blood mononuclear cells from bovine leukemia virus infected animals in the alymphocytotic disease stage express increased amount of IL-12 p40 mRNA. In contrast, IL-12 p40 mRNA expression by PL animals was significantly decreased compared to normal and alymphocytotic animals. To examine the functions of these cytokines on BLV expression, BLV tax and pol mRNA expression and p24 protein production were quantified by competitive PCR, and by immunoblotting, respectively. IL-10 inhibited BLV tax and pol mRNA expression by BLV-infected PBMCs. In addition, we determined that macrophages secret soluble factor(s) that activate BLV expression, and that secretion of the soluble factor(s) could be inhibited by IL-10. In contrast, IL-2 increased BLV tax and pol mRNA, and p24 protein production. These findings suggest that macrophages have a key role in regulating BLV expression, and IL-10 produced by BLV-infected animals in late disease stages may serve to control BLV expression, while IL-2 in the early stage of disease may activate BLV expression. PGE2 is an important immune regulator produced only by macrophages, and is known to facilitate HIV replication. We hypothesized that PGE2 may regulate BLV expression. Here, we show that cyclooxygenase-2 (COX-2) mRNA expression was decreased in PBMCs treated with IL-10, while IL-2 enhanced COX-2 mRNA expression. In contrast, addition of PGE2 stimulated BLV tax and pol mRNA expression. In addition, the specific COX-2 inhibitor, NS-398, inhibited BLV expression, while addition of PGE2 increased BLV tax expression regardless of NS-398. These findings suggest that macrophage derived cyclooxygenase -2 products, such as PGE2, may regulate virus expression and disease rogression in BLV infection, and that cytokines (IL-2 and IL-10) may regulate BLV expression through PGE2 production.
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