scholarly journals MiR-31 promotes Th22 differentiation through targeting Bach2 in coronary heart disease

2019 ◽  
Vol 39 (9) ◽  
Author(s):  
Rimao Huang ◽  
Xuliang Chen ◽  
Yadong Long ◽  
Ri Chen
Keyword(s):  
Coronary Heart Disease ◽  
T Cells ◽  
Heart Disease ◽  
Cd4 T Cells ◽  
Luciferase Reporter ◽  
Quantitative Real Time Pcr ◽  
Btb Domain ◽  
Aryl Hydrocarbon ◽  
Dual Luciferase Reporter Assay

Abstract The aim of the present study was to investigate the role of miR-31 in Th22 differentiation in coronary heart disease (CHD). Th22 frequencies in peripheral blood of CHD patients and controls as well as in CD4+ T cells were detected by flow cytometry. The mRNA expression of Th22-associated transcription factor aryl hydrocarbon receptor (AHR) and Th22-effector cytokine interleukin (IL)-22, as well as miR-31 were examined by quantitative real-time PCR (qRT-PCR). The protein level of BTB domain and CNC homolog 2 (Bach2) was measured by Western blotting. The interaction between miR-31 and Bach2 was verified using dual luciferase reporter assay. The results showed that Th22 frequency and miR-31 expression were elevated in CHD patients. Furthermore, miR-31 mimic and Bach2 silencing significantly promoted Th22 frequency and the levels of AHR and IL-22 in CD4+ T cells from CHD patients. Further studies showed that miR-31 facilitated Th22 cell differentiation by targeting and inhibiting Bach2. Our data indicate that miR-31 promotes Th22 differentiation through targeting Bach2 in CHD.

scholarly journals Role of MiR-98 and Its Underlying Mechanisms in Systemic Lupus Erythematosus

2018 ◽  
Vol 45 (10) ◽  
pp. 1397-1405 ◽  
Author(s):  
Lin Xie ◽  
Jinhua Xu
Keyword(s):  
T Cells ◽  
Lupus Erythematosus ◽  
Cd4 T Cells ◽  
Opposite Effect ◽  
Luciferase Reporter ◽  
Qrt Pcr ◽  
Fas Mrna ◽  
Reporter Assays ◽  
Underlying Mechanisms

Objective.T-lymphocyte apoptosis plays a critical role in the pathogenesis of systemic lupus erythematosus (SLE). However, the underlying regulatory mechanisms of apoptosis in SLE remain unclear. The aim of this study was to explore the role of miR-98 in SLE and its underlying mechanisms.Methods.Western blotting and quantitative reverse transcription PCR (qRT-PCR) were used to analyze miR-98 and Fas expression. Luciferase reporter assays were performed to identify miR-98 targets. To modify miRNA levels, miR-98 mimics and inhibitor were transfected into cells. A lentiviral construct was used to overexpress the level of Fas in SLE CD4+ T cells. Gene and protein expression were determined by qRT-PCR and Western blotting. Apoptosis levels were evaluated by annexin V staining and flow cytometry.Results.Compared to those of healthy donors, miR-98 was downregulated in SLE CD4+ T cells, whereas Fas mRNA and protein expression were upregulated. Upregulation of miR-98 by mimic transfection protected Jurkat cells against Fas-mediated apoptosis at both mRNA and protein levels, while miR-98 inhibitor induced the completely opposite effect. Luciferase reporter assays demonstrated that miR-98 directly targeted Fas mRNA. Further, miR-98 inhibitor induced apoptosis in primary healthy CD4+ T cells through the Fas-caspase axis, while upregulation of miR-98 in SLE CD4+ T cells led to the opposite effect.Conclusion.The current study revealed that downregulation of miR-98 induces apoptosis by modulating the Fas-mediated apoptotic signaling pathway in SLE CD4+ T cells. These results suggest that miR-98 might serve as a potential target for SLE treatment.

The role of CCR2+ CD4 T cells in lung fibrosis

Pneumologie ◽  
2014 ◽  
Vol 68 (S 01) ◽  
Author(s):  
K Milger ◽  
Y Yu ◽  
E Brudy ◽  
M Irmler ◽  
A Skapenko ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Lung Fibrosis

Modern ideas about the role of hyperuricemia in the pathogenesis of coronary heart disease

2018 ◽  
Vol 2 (1) ◽  
pp. 47-54
Author(s):  
Eleonora TASHKENBAEVA ◽  
◽  
Dilshod TOGAEV ◽  
Farzona KADIROVA ◽  
Shukhrat ZIYADULLAEV ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease

The Role of Mapalus Culture by Minahasa Ethnic in North Sulawesi to the Coronary Heart Disease Incidents

2018 ◽  
Vol 8 (3) ◽  
Author(s):  
Jeini Ester Nelwan ◽  
Edi Widjajanto ◽  
Sri Andarini ◽  
Sasmito Djati ◽  
Oksfriani Jufri Sumampouw
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
North Sulawesi

scholarly journals Ceramide Synthase 2 Null Mice Are Protected from Ovalbumin-Induced Asthma with Higher T Cell Receptor Signal Strength in CD4+ T Cells

2021 ◽  
Vol 22 (5) ◽  
pp. 2713
Author(s):  
Sun-Hye Shin ◽  
Kyung-Ah Cho ◽  
Hee-Soo Yoon ◽  
So-Yeon Kim ◽  
Hee-Yeon Kim ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Receptor ◽  
Cd4 T Cells ◽  
Acyl Chain ◽  
Signal Strength ◽  
Cell Receptor ◽  
Ceramide Synthase ◽  
Asthmatic Patients

(1) Background: six mammalian ceramide synthases (CerS1–6) determine the acyl chain length of sphingolipids (SLs). Although ceramide levels are increased in murine allergic asthma models and in asthmatic patients, the precise role of SLs with specific chain lengths is still unclear. The role of CerS2, which mainly synthesizes C22–C24 ceramides, was investigated in immune responses elicited by airway inflammation using CerS2 null mice. (2) Methods: asthma was induced in wild type (WT) and CerS2 null mice with ovalbumin (OVA), and inflammatory cytokines and CD4 (cluster of differentiation 4)+ T helper (Th) cell profiles were analyzed. We also compared the functional capacity of CD4+ T cells isolated from WT and CerS2 null mice. (3) Results: CerS2 null mice exhibited milder symptoms and lower Th2 responses than WT mice after OVA exposure. CerS2 null CD4+ T cells showed impaired Th2 and increased Th17 responses with concomitant higher T cell receptor (TCR) signal strength after TCR stimulation. Notably, increased Th17 responses of CerS2 null CD4+ T cells appeared only in TCR-mediated, but not in TCR-independent, treatment. (4) Conclusions: altered Th2/Th17 immune response with higher TCR signal strength was observed in CerS2 null CD4+ T cells upon TCR stimulation. CerS2 and very-long chain SLs may be therapeutic targets for Th2-related diseases such as asthma.

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