scholarly journals Altered expression of the DISC1 gene in peripheral blood of patients with schizophrenia

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Xiaoqian Fu ◽  
Guofu Zhang ◽  
Yansong Liu ◽  
Ling Zhang ◽  
Fuquan Zhang ◽  
...  
Keyword(s):  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Neuronal Morphology ◽  
Antipsychotic Treatment ◽  
Healthy Controls ◽  
Peripheral Blood Mononuclear ◽  
Expression Levels ◽  
Blood Mononuclear Cells ◽  
Before And After

Abstract Background Schizophrenia is a severe, heritable, and refractory psychiatric disorder. Several studies have shown that the disrupted in schizophrenia 1 (DISC1) gene is closely associated with schizophrenia by its role in neuronal morphology, synaptic function, brain development, and dopamine homeostasis etc. This study intended to investigate the expression levels of DISC1 gene in schizophrenia patients compared with healthy controls, and the expression variation of DISC1 gene before and after antipsychotic treatment in schizophrenia patients. Methods In this study, we compared DISC1 expression levels in blood of 48 healthy controls, and 32 schizophrenia patients before and after 12 weeks of antipsychotic treatment using real-time quantitative PCR (RT-qPCR) analysis. Results The expression levels of DISC1 gene in peripheral blood mononuclear cells of schizophrenia patients before antipsychotic treatment were higher than those in healthy controls (P < 0.01); whereas after antipsychotic treatment, the expression levels of DISC1 gene in peripheral blood mononuclear cells of schizophrenia patients still remained increased (P < 0.01). Conclusions Our study provided further support for the involvement of DISC1 in the development of schizophrenia.

Intraindividual variation of microRNA expression levels in plasma and peripheral blood mononuclear cells and the associations of these levels with the pathogenesis of autoimmune thyroid diseases

2017 ◽  
Vol 55 (5) ◽  
Author(s):  
Hiroshi Otsu ◽  
Mikio Watanabe ◽  
Naoya Inoue ◽  
Ryota Masutani ◽  
Yoshinori Iwatani
Keyword(s):  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Healthy Controls ◽  
Intraindividual Variation ◽  
Autoimmune Thyroid Diseases ◽  
Peripheral Blood Mononuclear ◽  
Expression Levels ◽  
Autoimmune Thyroid ◽  
Blood Mononuclear Cells

AbstractBackground:microRNAs (miRNAs) circulate in the blood and negatively regulate the expression of mRNAs. Some miRNAs are associated with the development of autoimmune thyroid diseases (AITD); however, there are few reports on the association between miRNA expression and the pathogenesis of AITD or the physiological variations of circulating miRNAs, which are important to examine as biomarkers.Methods:We examined the circadian and day-to-day variations in the expression levels of 5 miRNAs (miR-125a, miR-146a, miR-155, let-7e and miR-106a) in plasma and peripheral blood mononuclear cells (PBMC). We also analysed the expression levels of two of these miRNAs (miR-146a and miR-155) in 20 healthy controls, 60 Graves’ disease (GD) patients and 50 Hashimoto’s disease (HD) patients.Results:For each miRNA, we observed wide intraindividual variation [coefficient of variation value (CV): 70%–100%] compared to measurement error (CV: 20%–40%). In patients with AITD, HD, GD in remission and mild HD, the expression levels of miR-146a in PBMC were increased 296%, 328%, 348% and 464% above the levels in healthy controls, respectively (p=0.0443 and p=0.0273, p=0.0267 and p=0.0052, respectively). In severe HD, the expression level of miR-155 in plasma was increased to 347% of that in healthy controls (p=0.0256).Conclusions:The expression levels of miRNAs in plasma and PBMC showed wide intraindividual variation. In addition, miR-146a may be associated with the development of AITD.

scholarly journals AB0011 EXPRESSION PROFILE AND POTENTIAL FUNCTION OF CIRCRNAS IN PERIPHERAL BLOOD MONONUCLEAR CELLS FROM PATIENTS WITH PRIMARY GOUT

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1040.2-1040
Author(s):  
Y. F. Qing ◽  
F. Dai ◽  
Q. B. Zhang ◽  
Y. P. Tang ◽  
Z. R. Dong ◽  
...  
Keyword(s):  
Blood Cell ◽  
Peripheral Blood Mononuclear Cells ◽  
Red Blood Cell ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Research Support ◽  
Peripheral Blood Mononuclear ◽  
Expression Levels ◽  
Blood Mononuclear Cells ◽  
Before And After

Background:Autophagy is a phenomenon of “self-phagocytosis” in eukaryotic cells, which maintains cell homeostasis by transporting intracellular materials to lysosomes for degradation and recycling. In recent years, studies have shown that autophagy may be involved in the pathogenesis of rheumatoid arthritis(RA)[1], but its specific mechanism is still unclear.Objectives:The expression levels of autophagy-related genes(ATG) unc-51-like kinase 1(ULK1), ATG13, ATG17, microtubule associated protein 1 light chain 3 (LC3), and P62 in peripheral blood mononuclear cells (PBMC) of patients with RA were detected, and their role and clinical significance in the pathogenesis of RA were explored.Methods:Real-time fluorescent quantitative PCR was performed to detect the expression levels of ULK1, ATG13, ATG17, LC3, and P62 in PBMCs of 50 RA patients, 50 healthy controls (HC), and 25 moderate to severe RA patients before and after treatment. Then, t test, χ2 test, Mann-Whitney U test, Pearson test were used for statistical analysis.Results:1.The levels of hsCRP, white blood cell(WBC), neutrophils(GR), platelet(PLT) and plateletcrit(PCT) in RA group were higher than those in HC group (P <0.05). Lymphocytes (LY), red blood cell(RBC), hemoglobin(HGB), hematocrit(HCT), mean corpuscular hemoglobin(MCH), mean red blood cell volume(MCV) and mean red blood cell hemoglobin concentration(MCHC) in RA group were lower than those in HC group (P <0.05). 2.The expressions of ULK1, ATG17, and LC3 in RA group were higher than those in HC group, while the expressions of P62 was lower than those in HC group(P<0.05) (Figure 1). The correlation analysis suggested that ATG17 was positively correlated with tender joint count (TJC), swollen joint count (SJC), and health assessment questionnaire (HAQ) (P<0.05); ULK1 and HAQ were negatively correlated (P<0.05).3. Compared with before treatment with TNFi, ATG17, HAQ, DAS-28, ESR, hsCRP, WBC, GR, PLT and PCT were significantly reduced after treatment (P<0.05); the expressions of RBC, HCT, MCV and MCH were significantly increased after treatment,(P<0.05); ULK1, ATG13, LC3, P62 and other related clinical and laboratory indicators were not significantly different before and after treatment with TNFi (P>0.05).Figure 1.The expression levels of ATGs in HC and RA groups.Conclusion:There is abnormal expression of autophagy genes in the peripheral blood of RA patients. ULK1, ATG17, LC3 and P62 may be related to the pathogenesis of RA, among them, ATG17 may regulate the pathogenesis of RA by participating in the TNF-α pathway.References:[1]Rockel Jason S,Kapoor Mohit,Autophagy: controlling cell fate in rheumatic diseases.[J].Nat Rev Rheumatol, 2016, 12: 517-31.Disclosure of Interests:Yu-Feng Qing Grant/research support from: Science and Technology Project of Nanchong City (no.18SXHZ0522), Fei Dai: None declared, Quan-Bo Zhang Grant/research support from: the National Natural Science Foundation of China(General Program) (no.81974250), and Science and Technology Plan Project of Sichuan Province (no.2018JY0257), Yi-Ping Tang: None declared, Zeng-Rong Dong: None declared, Yi-Xi He: None declared, Yi Jiang: None declared, Yu-Qin Huang: None declared, Jianxiong Zheng: None declared

scholarly journals The Expression and Pathophysiological Role of Osteopontin in Graves' Disease

2011 ◽  
Vol 96 (11) ◽  
pp. E1866-E1870 ◽  
Author(s):  
Lingyan Xu ◽  
Xinran Ma ◽  
Yanyan Wang ◽  
Xiaoli Li ◽  
Yicheng Qi ◽  
...  
Keyword(s):  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Graves Disease ◽  
Healthy Controls ◽  
Peripheral Blood Mononuclear ◽  
Pathophysiological Role ◽  
Blood Mononuclear Cells

Abstract Context: Graves' disease (GD) is a common autoimmune disease that affects the thyroid gland. Its pathogenesis is tightly involved with aberrant proinflammatory cytokine production. Osteopontin (OPN), an extracellular matrix protein of pleiotropic properties, has recently been recognized as a potent inflammatory cytokine in several autoimmune diseases. Objective: This study sought to explore the pathophysiological role of OPN in GD by comparing OPN levels in initial GD patients and healthy controls. Methods: Seventy-six patients who met criteria for initial GD and sixty-five healthy controls were recruited. OPN and other clinical GD diagnosis parameters were measured. In addition, the coexpression of several OPN receptors as well as various nuclear factor-κB (NF-κB) downstream target genes were examined in peripheral blood mononuclear cells from human subjects. The effect of OPN on NF-κB activation was determined by in vitro assays. Results: We demonstrated for the first time that the OPN levels are enhanced in serum from GD patients. OPN levels are strongly associated with clinical serum parameters for GD diagnosis. The coexpression of selective OPN receptors and inflammatory response genes was enhanced in peripheral blood mononuclear cells from GD patients. Furthermore, serum from GD patients activated NF-κB activity in vitro, which was significantly suppressed by OPN monoclonal antibody abrogation. Conclusion: These data indicated a clinical correlation between serum OPN levels and GD. OPN could affect GD development through NF-κB activation and the subsequent changes in inflammatory milieu. OPN could serve as a novel biomarker for GD as well as a potential target for GD treatment.

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