scholarly journals miR-19a and miR-20a and Tissue Factor Expression in Activated Human Peripheral Blood Mononuclear Cells

Thrombosis ◽  
2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Cristina Balia ◽  
Mirella Giordano ◽  
Valentina Scalise ◽  
Tommaso Neri ◽  
Gabriella Fontanini ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Peripheral Blood Mononuclear Cells ◽  
High Glucose ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells ◽  
Inflammatory Stimuli

Background and Aims. To investigate the behaviour of miR-19a and miR-20a, two microRNAs involved in posttranscriptional modulation of TF expression in peripheral blood mononuclear cells (PBMCs) exposed to high glucose (HG) and lipopolysaccharide (LPS), and to evaluate the involvement of angiotensin II in that process. Methods. TF Procoagulant Activity (PCA, one-stage clotting assay), antigen (Ag, ELISA), and miR-19a and miR-20a levels (specific TaqMan® MicroRNA Assays) were evaluated in PBMCs exposed to high glucose (HG, 50 mM), LPS (100 ng/mL), and Olmesartan (OLM, 10−6 M), an angiotensin II type 1 receptor antagonist. Results. HG increased TF expression and decreased both miRs as compared to control glucose conditions (11.1 mM). In HG-activated PBMCs, LPS stimulated TF expression and downregulated miR-20a, an effect reverted by OLM (10−6 M); miR-19a expression was unchanged by LPS in both CG and HG conditions. Conclusions. miR-19a and miR-20a are inhibited by inflammatory stimuli active on TF expression and their response differs by the stimulus under investigation; angiotensin II may participate in that mechanism.

Sendai Virus and Herpes Virus Type 1 Induce Apoptosis in Human Peripheral Blood Mononuclear Cells

1995 ◽  
Vol 218 (1) ◽  
pp. 63-70 ◽  
Author(s):  
Franco Tropea ◽  
Leonarda Troiano ◽  
Daniela Monti ◽  
Elena Lovato ◽  
Walter Malorni ◽  
...  
Keyword(s):  
Virus Type ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Sendai Virus ◽  
Human Peripheral Blood ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells ◽  
Herpès Virus

HTLV-1 p12I protein enhances STAT5 activation and decreases the interleukin-2 requirement for proliferation of primary human peripheral blood mononuclear cells

Blood ◽  
2001 ◽  
Vol 98 (3) ◽  
pp. 823-829 ◽  
Author(s):  
Christophe Nicot ◽  
James C. Mulloy ◽  
Maria G. Ferrari ◽  
Julie M. Johnson ◽  
Kaisong Fu ◽  
...  
Keyword(s):  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Interleukin 2 ◽  
Peripheral Blood Mononuclear ◽  
Low Concentrations ◽  
Blood Mononuclear Cells ◽  
Proliferative Advantage

Abstract The p12I protein, encoded by the pX open reading frame I of the human T-lymphotropic virus type 1 (HTLV-1), is a hydrophobic protein that localizes to the endoplasmic reticulum and the Golgi. Although p12I contains 4 minimal proline-rich, src homology 3–binding motifs (PXXP), a characteristic commonly found in proteins involved in signaling pathways, it has not been known whether p12I has a role in modulating intracellular signaling pathways. This study demonstrated that p12I binds to the cytoplasmic domain of the interleukin-2 receptor (IL-2R) β chain that is involved in the recruitment of the Jak1 and Jak3 kinases. As a result of this interaction, p12I increases signal transducers and activators of transcription 5 (STAT5) DNA binding and transcriptional activity and this effect depends on the presence of both IL-2R β and γc chains and Jak3. Transduction of primary human peripheral blood mononuclear cells (PBMCs) with a human immunodeficiency virus type 1–based retroviral vector expressing p12I also resulted in increased STAT5 phosphorylation and DNA binding. However, p12I could increase proliferation of human PBMCs only after stimulation of T-cell receptors by treatment of cells with low concentrations of αCD3 and αCD28 antibodies. In addition, the proliferative advantage of p12I-transduced PBMCs was evident mainly at low concentrations of IL-2. Together, these data indicate that p12I may confer a proliferative advantage on HTLV-1–infected cells in the presence of suboptimal antigen stimulation and that this event may account for the clonal proliferation of infected T cells in vivo.

Regulatory Effects of High Glucose on the Expression of Toll-Like Receptor Gene and Cytokine Production in Human Peripheral-Blood Mononuclear Cells

2011 ◽  
Vol 179-180 ◽  
pp. 374-379 ◽  
Author(s):  
Jing Sheng Lan ◽  
Yu Kang Dong ◽  
Xing Ming Cai
Keyword(s):  
Peripheral Blood Mononuclear Cells ◽  
High Glucose ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Toll Like Receptor ◽  
Peripheral Blood Mononuclear ◽  
Tnf Α ◽  
Blood Mononuclear Cells ◽  
Regulatory Effects

To investigate the regulatory effects of high glucose on the expression of Toll Like Receptor(TLR) Gene and the level of tumor necrosis factor(TNF)-α and interleukin(IL) -6 in human peripheral-blood mononuclear cells . Methods The alterations of TLR1～10 mRNA expression in human peripheral-blood mononuclear cells were quantitated using real-time quantitative-polymerasechain reaction. The level of TNF-α and IL-6 were measured by Enzyme-Linked Immuno Sorbent Assay . The anti-TLRmAb were used to block the mononuclear cells 30 min, high glucose was used to stimulate the cells. Rusults high glucose strongly up-regulated the expression of TLR3、5 mRNA but the expression of the other sub-TLRs weren’t changed .The concentrations of TNF-α、IL-6 were 86.40±8.46 and 874.66±92.84 in high glucose group, all significantly higher than that the control experiment (60.49±6.80 and 541.80±81.08 , all P<0.01), The anti-TLR3mAb and anti-TLR5mAb were used to block the mononuclear cells , The concentrations of TNF-α、IL-6 (72.41±8.52 and 700.59±84.88) were lower than that in the high glucose group, all P<0.05 . Conclusion high glucose may be endogenous ligand of TLRs and high glucose can regulate the release of inflammation cytokines from human peripheral-blood mononuclear cells through TLR signal way.

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