scholarly journals Bulky DNA adducts, microRNA profiles, and lipid biomarkers in Norwegian tunnel finishing workers occupationally exposed to diesel exhaust

2018 ◽  
Vol 76 (1) ◽  
pp. 10-16 ◽  
Author(s):  
Iselin Rynning ◽  
Volker M Arlt ◽  
Kristyna Vrbova ◽  
Jiří Neča ◽  
Pavel Rossner Jr ◽  
...  
Keyword(s):  
Occupational Exposure ◽  
Dna Adducts ◽  
Diesel Exhaust ◽  
Mononuclear Cells ◽  
Mirna Gene ◽  
Small Rna Sequencing ◽  
Peripheral Blood Mononuclear ◽  
Occupationally Exposed ◽  
Bulky Dna Adducts ◽  
Heavy Duty Diesel

ObjectivesThis study aimed to assess the biological impact of occupational exposure to diesel exhaust (DE) including DE particles (DEP) from heavy-duty diesel-powered equipment in Norwegian tunnel finishing workers (TFW).MethodsTFW (n=69) and referents (n=69) were investigated for bulky DNA adducts (by 32P-postlabelling) and expression of microRNAs (miRNAs) (by small RNA sequencing) in peripheral blood mononuclear cells (PBMC), as well as circulating free arachidonic acid (AA) and eicosanoid profiles in plasma (by liquid chromatography–tandem mass spectrometry).ResultsPBMC from TFW showed significantly higher levels of DNA adducts compared with referents. Levels of DNA adducts were also related to smoking habits. Seventeen miRNAs were significantly deregulated in TFW. Several of these miRNAs are related to carcinogenesis, apoptosis and antioxidant effects. Analysis of putative miRNA-gene targets revealed deregulation of pathways associated with cancer, alterations in lipid molecules, steroid biosynthesis and cell cycle. Plasma profiles showed higher levels of free AA and 15-hydroxyeicosatetraenoic acid, and lower levels of prostaglandin D2 and 9-hydroxyoctadecadienoic acid in TFW compared with referents.ConclusionOccupational exposure to DE/DEP is associated with biological alterations in TFW potentially affecting lung homoeostasis, carcinogenesis, inflammation status and the cardiovascular system. Of particular importance is the finding that tunnel finishing work is associated with an increased level of DNA adducts formation in PBMC.

32P-Post-labeling detection of DNA adducts in mononuclear cells of workers occupationally exposed to styrene

1994 ◽  
Vol 15 (7) ◽  
pp. 1309-1315 ◽  
Author(s):  
Eva Horvath ◽  
Krisztina Pongracz ◽  
Stephen Rappaport ◽  
William J. Bodell
Keyword(s):  
Dna Adducts ◽  
Mononuclear Cells ◽  
Occupationally Exposed

PBMCs-Derived microRNA Signature as a Prethrombotic Status Discriminator in Stable Coronary Artery Disease

2019 ◽  
Vol 120 (01) ◽  
pp. 121-131 ◽  
Author(s):  
Jie Gao ◽  
Jia Liu ◽  
Ying Zhang ◽  
BaoYi Guan ◽  
Hua Qu ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Mononuclear Cells ◽  
Coronary Thrombosis ◽  
Stable Coronary Artery Disease ◽  
Mirna Gene ◽  
Healthy Controls ◽  
Diagnostic Significance ◽  
Peripheral Blood Mononuclear ◽  
Artery Disease

AbstractPrethrombotic status (PTS) in patients with stable coronary artery disease (SCAD) increases the risk of coronary thrombosis. Accumulating evidences have indicated that micro-ribonucleic acids (miRNAs) may serve as promising biomarkers for SCAD patients with PTS. The present study aimed to identify the miRNA signature in SCAD patients with PTS and evaluated their diagnostic significance. In the screening phase, 32 differently expressed miRNAs (DEMs) in peripheral blood mononuclear cells (PBMCs) were detected in 35 SCAD patients compared with 5 healthy controls by microarray. MiRNA-gene network analysis was then performed, and 4 DEMs were selected for validation with reverse transcription-quantitative real-time polymerase chain reaction (RT-qPCR) test in an independent cohort comprising 79 SCAD patients and 19 healthy controls. Compared with healthy controls, RT-qPCR test verified the upregulations of miR-34a-5p, miR-432–5p, and miR-370–3p detected by microarray; while the upregulation of miR-495–3p measured by RT-qPCR was not consistent with its low expression detected by microarray. Only miR-34a-5p and miR-495–3p were significantly upregulated in the PTS group compared with the non-PTS group (p < 0.01, p < 0.05). Receiver-operating characteristic (ROC) analysis showed that PBMCs-derived miR-34a-5p and miR-495–3p may discriminate PTS with the areas under the ROC curve (AUC) of 0.780 (confidence interval [CI]95% = 0.673–0.866) and 0.712 (CI95% = 0.599–0.808), respectively. The combination of miR-34a-5p and fibrinogen (FIB, a traditional biomarker for PTS) improved AUC to 0.885 (CI95% = 0.793–0.946) and showed added predictive ability compared with FIB, with an integrated discrimination improvement of 0.201 (p < 0.01). Therefore, the combination of miR-34a-5p and FIB may serve as an efficient tool for distinguishing PTS in SCAD patients.

Lead Impairs the Development of Innate Lymphoid Cells by Impeding the Differentiation of Their Progenitors

2020 ◽  
Vol 176 (2) ◽  
pp. 410-422 ◽  
Author(s):  
Tingting Zhu ◽  
Yifan Zhao ◽  
Peng Zhang ◽  
Yiming Shao ◽  
Jinyi He ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mononuclear Cells ◽  
Human Subjects ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
In Vitro Assays ◽  
Peripheral Blood Mononuclear ◽  
Occupationally Exposed ◽  
Pb Exposure

Abstract Lead (Pb) is a heavy metal toxic to the immune system, yet the influence of Pb on innate lymphoid cells (ILC) remains to be defined. In this study, we found that occupationally relevant level of Pb exposure impaired ILC development at the progenitor level by activating Janus Kinase1. C57BL/6 mice treated with 1250 ppm, but not 125 ppm Pb acetic via drinking water for 8 weeks had reduced number of mature ILC, which was not caused by increased apoptosis or suppressed proliferation. Conversely, Pb increased the number of innate lymphoid cell progenitors (ILCP) in the bone marrow. The discordant observation indicated that an obstruction of ILCP differentiation into mature ILC during Pb exposure existed. Pb directly acted on ILCP to suppress their proliferation, indicating that ILCP were less activated during Pb exposure. Reciprocal ILCP transplantation assay confirmed that Pb impeded the differentiation of ILCP into mature ILC, as ILCP gave rise to fewer mature ILC in Pb-treated recipients compared with control recipients. In vitro assays suggested that the obstruction of ILCP differentiation by Pb exposure was due to increased activation of Janus Kinase1. Thus, Pb impeded ILCP differentiation into mature ILC to result in an accumulation of ILCP in the bone marrow and the resultant decreased number of mature ILC in lymphoid and nonlymphoid tissues in mice. Moreover, by analyses of ILC and ILCP in peripheral blood mononuclear cells of human subjects occupationally exposed to Pb, we revealed that Pb might also impede the development of ILC in human.

scholarly journals Gene expression changes in peripheral blood mononuclear cells in occupational exposure to nickel

2010 ◽  
Vol 20 (2) ◽  
pp. 147-148 ◽  
Author(s):  
Serena Bonin ◽  
Francesca Filon Larese ◽  
Giusto Trevisan ◽  
Andrea Avian ◽  
Francesca Rui ◽  
...  
Keyword(s):  
Gene Expression ◽  
Occupational Exposure ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells

scholarly journals Long Non-Coding RNAs Modulate Sjögren’s Syndrome Associated Gene Expression and Are Involved in the Pathogenesis of the Disease

2019 ◽  
Vol 8 (9) ◽  
pp. 1349 ◽  
Author(s):  
Dolcino ◽  
Tinazzi ◽  
Vitali ◽  
Papa ◽  
Puccetti ◽  
...  
Keyword(s):  
Sjögren’S Syndrome ◽  
Mononuclear Cells ◽  
Sjögren's Syndrome ◽  
Mirna Gene ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Type I ◽  
Peripheral Blood Mononuclear ◽  
Non Coding Rnas ◽  
Sjögren‘S Syndrome

Primary Sjögren’s syndrome (pSjS) is a chronic systemic autoimmune disorder, primarily affecting exocrine glands; its pathogenesis is still unclear. Long non-coding RNAs (lncRNAs) are thought to play a role in the pathogenesis of autoimmune diseases and a comprehensive analysis of lncRNAs expression in pSjS is still lacking. To this aim, the expression of more than 540,000 human transcripts, including those ascribed to more than 50,000 lncRNAs is profiled at the same time, in a cohort of 16 peripheral blood mononuclear cells PBMCs samples (eight pSjS and eight healthy subjects). A complex network analysis is carried out on the global set of molecular interactions among modulated genes and lncRNAs, leading to the identification of reliable lncRNA-miRNA-gene functional interactions. Taking this approach, a few lncRNAs are identified as targeting highly connected genes in the pSjS transcriptome, since they have a major impact on gene modulation in the disease. Such genes are involved in biological processes and molecular pathways crucial in the pathogenesis of pSjS, including immune response, B cell development and function, inflammation, apoptosis, type I and gamma interferon, epithelial cell adhesion and polarization. The identification of deregulated lncRNAs that modulate genes involved in the typical features of the disease provides insight in disease pathogenesis and opens avenues for the design of novel therapeutic strategies.

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