scholarly journals Cholesterol Transporters ABCA1 and ABCG1 Gene Expression in Peripheral Blood Mononuclear Cells in Patients with Metabolic Syndrome

Cholesterol ◽  
2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Zahra Tavoosi ◽  
Hemen Moradi-Sardareh ◽  
Massoud Saidijam ◽  
Reza Yadegarazari ◽  
Shiva Borzuei ◽  
...  

ABCA1 and ABCG1 genes encode the cholesterol transporter proteins that play a key role in cholesterol and phospholipids homeostasis. This study was aimed at evaluating and comparing ABCA1 and ABCG1 genes expression in metabolic syndrome patients and healthy individuals. This case-control study was performed on 36 patients with metabolic syndrome and the same number of healthy individuals in Hamadan (west of Iran) during 2013-2014. Total RNA was extracted from mononuclear cells and purified using RNeasy Mini Kit column. The expression of ABCA1 and ABCG1 genes was performed by qRT-PCR. Lipid profile and fasting blood glucose were measured using colorimetric procedures. ABCG1 expression in metabolic syndrome patients was significantly lower (about 75%) compared to that of control group, while for ABCA1 expression, there was no significant difference between the two studied groups. Comparison of other parameters such as HDL-C, FBS, BMI, waist circumference, and systolic and diastolic blood pressure between metabolic syndrome patients and healthy individuals showed significant differences (P<0.05). Decrease in ABCG1 expression in metabolic syndrome patients compared to healthy individuals suggests that hyperglycemia, related metabolites, and hyperlipidemia over the transporter capacity resulted in decreased expression of ABCG1. Absence of a significant change in ABCA1 gene expression between two groups can indicate a different regulation mechanism for ABCA1 expression.

2008 ◽  
Vol 158 (4) ◽  
pp. 499-510 ◽  
Author(s):  
Ursula Mager ◽  
Marjukka Kolehmainen ◽  
Vanessa D F de Mello ◽  
Ursula Schwab ◽  
David E Laaksonen ◽  
...  

ObjectiveWe examined the expression of ghrelin and ghrelin receptors in peripheral blood mononuclear cells (PBMCs) and evaluated the effect of weight loss or exercise on plasma ghrelin concentrations in subjects with the metabolic syndrome.Design and methodsData from 75 overweight/obese subjects randomized to a weight loss, aerobic exercise, resistance exercise or control group for a 33-week intervention period were analysed. The plasma ghrelin concentrations and indices of insulin and glucose metabolism were assessed, and mRNA expression of ghrelin, its receptors and various cytokines in PBMCs was studied using real-time PCR.ResultsGhrelin and GH secretagogue receptor 1b were expressed in PBMCs of subjects with metabolic syndrome. Ghrelin gene expression correlated positively with the expressions of tumour necrosis factor-α (P<0.001), interleukin-1β (P<0.001) and interleukin-6 (P=0.026) during the study, but was not associated with the plasma ghrelin concentration. Genotype-specific ghrelin gene expression in PBMCs was found for the −604G/A and the −501A/C polymorphisms in the ghrelin gene. At baseline, the plasma ghrelin levels were associated with fasting serum insulin concentrations, insulin sensitivity index and high-density lipoprotein cholesterol. However, longitudinally weight, BMI or waist circumference and acute insulin response in i.v. glucose tolerance test were stronger predictors of the ghrelin concentration. Plasma ghrelin did not change over the study period in the weight reduction group, but it tended to decrease in the control group (P=0.050).ConclusionsGhrelin mRNA expression in PBMCs suggests an autocrine role for ghrelin within an immune microenvironment. Moderate long-term weight loss may prevent a decline in ghrelin concentration over time in individuals with metabolic syndrome.


Author(s):  
Thaslima Nandhini Js ◽  
Savitha Basker G ◽  
Vishnupriya V

Objective: Metabolic syndrome is a cluster of disease condition characterized by truncal obesity, hypertriglyceridemia, elevated blood pressure, and insulin resistance. An excessive circulating uric acid (UA) level even within normal range is always comorbid with metabolic syndrome and its components. The aim of the current study was to investigate the association between metabolic syndrome and serum UA level.Methods: A total of 60 subjects were divided into two groups of healthy (30 individuals) and metabolic syndrome patients (30 individuals) from dental outpatient department of Saveetha Dental College and Hospitals. 5 ml of fasting venous blood was collected in the plain collection tubes and centrifuged, and then serum was separated. Then, the serum was used to analyze the fasting blood glucose, serum triglycerides (TGLs), and serum UA by GOD-POD, enzymatic colorimetric, and uricase method, respectively. A statistical analysis was performed using Student’s t-test. p<0.05 was considered to be statistically significant.Result: Mean body mass index (BMI), fasting blood sugar (FBS), TGL, and UA level of control group were 23.36±1.81, 84.45±13.1, 110.9±22.6, and 3.48±1.21 respectively. Mean BMI, FBS, TGL, and UA level of study group were 35.24±3.04, 122.85±23.3, 212.1±39.6 and 9.08±2.63 respectively. There is a significant difference between these two groups with p<0.0001.Conclusion: This study showed that those individuals with metabolic syndrome have higher UA level that indicates hyperuricemia which is a significant predictor of metabolic syndrome.


2020 ◽  
Author(s):  
A Andrianto ◽  
Adityo Basworo ◽  
Ivana Purnama Dewi ◽  
Budi Susetio Pikir

IntroductionIt is possible to induce pluripotent stem cells from somatic cells, offering an infinite cell resource with the potential for disease research and use in regenerative medicine. Due to ease of accessibility, minimum invasive treatment, and can be kept frozen, peripheral blood mononuclear cells (PBMC) were an attractive source cell. VC6TFZ, a small molecule compound, has been successfully reprogrammed from mouse fibroblast induced pluripotent stem cells (iPSCs). However, it has not been confirmed in humans.ObjectiveThe aim of this research is to determine whether the small molecule compound VC6TFZ can induced pluripotency of PBMC to generate iPSCs detected with expression of SSEA4 and TRA1-60.MethodsUsing the centrifugation gradient density process, mononuclear cells were separated from peripheral venous blood. Mononuclear cells were cultured for 6 days in the expansion medium. The cells were divided into four groups; group 1 (P1), which was not exposed to small molecules (control group) and groups 2-4 (P2-P4), the experimental groups, subjected to various dosages of the small molecule compound VC6TFZ (VPA, CHIR, Tranylcypromine, FSK, Dznep, and TTNPB). The induction of pluripotency using small molecule compound VC6TFZ was completed within 14 days, then for 7 days the medium shifted to 2i medium. iPSCs identification in based on colony morphology and pluripotent gene expression, SSEA4 and TRA1-60 marker, using immunocytochemistry.ResultsColonies appeared on reprogramming process in day 7th. These colonies had round, large, and cobble stone morphology like ESC. Gene expression of SSEA4 and TRA 1-60 increased statisticaly significant than control group (SSEA4 were P2 p=0.007; P3 p=0.001; P4 p=0.009 and TRA 1-60 were P2 p=0.002; P3 p=0.001; P4 p=0.001).ConclusionSmall molecule compound VC6TFZ could induced pluripotency of human PBMC to generate iPSCs. Pluripotxency marker gene expression, SSEA 4 and TRA 1-60, in the experimental group was statistically significantly higher than in the control group.


Nutrients ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 2932 ◽  
Author(s):  
Stine M. Ulven ◽  
Kirsten B. Holven ◽  
Amanda Rundblad ◽  
Mari C. W. Myhrstad ◽  
Lena Leder ◽  
...  

A healthy dietary pattern is associated with a lower risk of metabolic syndrome (MetS) and reduced inflammation. To explore this at the molecular level, we investigated the effect of a Nordic diet (ND) on changes in the gene expression profiles of inflammatory and lipid-related genes in peripheral blood mononuclear cells (PBMCs) of individuals with MetS. We hypothesized that the intake of an ND compared to a control diet (CD) would alter the expression of inflammatory genes and genes involved in lipid metabolism. The individuals with MetS underwent an 18/24-week randomized intervention to compare a ND with a CD. Eighty-eight participants (66% women) were included in this sub-study of the larger SYSDIET study. Fasting PBMCs were collected before and after the intervention and changes in gene expression levels were measured using TaqMan Array Micro Fluidic Cards. Forty-eight pre-determined inflammatory and lipid related gene transcripts were analyzed. The expression level of the gene tumor necrosis factor (TNF) receptor superfamily member 1A (TNFRSF1A) was down-regulated (p = 0.004), whereas the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) subunit, RELA proto-oncogene, was up-regulated (p = 0.016) in the ND group compared to the CD group. In conclusion, intake of an ND in individuals with the MetS may affect immune function.


2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Yanhong Sun ◽  
Xiaoyan Wan ◽  
Juan Ouyang ◽  
Renfeng Xie ◽  
Xueping Wang ◽  
...  

Objective. Prenatal glucocorticoids (GC) can induce long term effects on offspring health. However, reports and related studies regarding the prolonged effects of prenatal GC on the development of autoimmunity are limited. Here, we aimed to explore the immunological effects of dexamethasone (DEX) exposure on young adults and whether glucocorticoid receptor (GR) is involved in this process. Methods. Wistar rats were given DEX during pregnancy. Susceptibility to autoimmunity in offspring was assessed using experimental autoimmune encephalomyelitis (EAE) and adjuvant-induced arthritis (AIA) animal models. To reveal the possible mechanism, glucocorticoid response, GR expression, and methylation status were measured in peripheral blood mononuclear cells (PBMCs). Results. Our results showed that the DEX-treated rats had greater susceptibility to EAE (100% versus 62.5%, P<0.05) and AIA (63.6% versus 0%, P<0.05) than saline control group. Glucocorticoid response and GR expression were decreased in DEX rats. Significant difference was also found in the methylation levels of GR exon 1-10 to exon 1-11 region. Conclusions. Prenatal DEX administration increases the susceptibility to autoimmune diseases, which is potentially mediated by programming GR methylation status and glucocorticoid sensitivity.


Author(s):  
Agata Krawczyk ◽  
Barbara Strzałka-Mrozik ◽  
Dominika Wcisło-Dziadecka ◽  
Magdalena Kimsa-Dudek ◽  
Celina Kruszniewska-Rajsa ◽  
...  

IntroductionThe primary goal of psoriasis treatment is to reduce the inflammatory response and associated complications. In severe cases of psoriasis that are resistant to local treatment (e.g., keratolytic preparations) and at least two types of general treatment methods (e.g., retinoids and cyclosporine A), biological therapy is used. This study aimed to assess the systemic effects of adalimumab at a given stage of treatment in patients with psoriatic arthritis and evaluate how the drug can improve the clinical condition of the patients.Material and methodsThe study group consisted of patients with diagnosed psoriatic arthritis, while the control group consisted of individuals from whom peripheral blood mononuclear cells were obtained. The effects of the administration of adalimumab were assessed by analyzing the gene expression using oligonucleotide microarrays.ResultsThe apoptosis process was indicated as one of the overrepresented categories (the PANTHER classification system 13.1 program, overrepresentativity test, p < 0.05). The dermatological indexes decreased, indicating an improvement in the clinical conditions of the patients three months after the first dose of adalimumab.ConclusionsWe found that adalimumab affects apoptosis, which is crucial in the development and course of psoriasis. The differential gene expression in peripheral blood mononuclear cells of patients with psoriatic arthritis indicated the potential systemic effects of adalimumab therapy. The analyses of dermatological (the Psoriasis Area And Severity Index, body surface area and Dermatology Life Quality Index) and inflammatory (Biernacki’s reaction) parameters revealed the effectiveness of the therapy.


2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e13001-e13001
Author(s):  
Ioannis Papasotiriou ◽  
Dimitrios Ntanovasilis ◽  
Panagiotis Apostolou

e13001 Background: A variety of chromosomal aberrations underlie developmental abnormalities and cancer. Use of techniques such as microarrays provides an opportunity to perform gene expression analysis. A recent approach is the use of array based comparative genomic hybridization (aCGH) to detect genomic abnormalities in human tumors. The aim of this study is to compare genomic and gene expression profile between cancer patients and healthy individuals. Methods: DNA and RNA were isolated from peripheral blood mononuclear cells from 9 patients, with different types of cancer and 4 normal donors. aCGH (Agilent-60K) and gene expression microarrays (Microarrays Inc.-whole genome platform) were performed using commercial reference samples. Data were analyzed with Array-Pro analyzer and Cytogenomics software. Results: The aCGH data demonstrated the majority of gains and amplifications were observed in cancer samples, while the deletions and losses were higher in normal individuals. Among aberrations, common genes in both types of samples were detected. These genes included ACAD8, ACP1, B3GAT1, IDI1, IDI2, IGSF9B, IRX1, IRX2, JAM3, MYT1L, NTM, OPCML, PXDN, THYN1, TPO. However, there were abnormalities that included genes, which appeared only in cancer samples, like cadherins ( CDH11, CDH8 and CDH5) and EPHA5, while genes such as ACOX1, PTPRN2, TYMS and genes of zinc-finger proteins were observed only in normal samples. No statistical significant difference in gene expression, between cancer and normal samples, was observed. On the contrary, overexpression was observed in genes that were not detected in aCGH. Conclusions: Whereas it is acceptable that great achievements have been carried out in cancer field, the mechanism of tumorigenesis is not clear understood. The present study demonstrated that even though genomic aberrations exist, these are not always representative at gene expression level. However, the combination of both techniques could be used for more accurate and reliable data. This requires study in more samples including different cancer types so to be used at clinical level.


2015 ◽  
Vol 2015 ◽  
pp. 1-4 ◽  
Author(s):  
Seyran Ozbas Gok ◽  
Asli Akin Belli ◽  
Emine Dervis

Background.There are several studies investigating the relationship between androgenetic alopecia (AGA) and metabolic syndrome (MS) with conflicting results.Objective.We sought to investigate whether there is a relationship between AGA and MS.Methods.A case-control study including 74 male patients with AGA and 42 male controls was conducted. Age, duration of AGA, AGA onset age, anthropometric measures, body mass index, lipid parameters, fasting blood glucose, blood pressure, and presence of MS were recorded.Results.Of the 74 male AGA patients (age range 20–50 years, mean 32.14), 24 were in stage 2, 26 were in stage 3, 17 were in stage 3V, 1 was in stage 5, and 6 were in stage 7. There was no significant difference in the rate of MS between AGA and control groups(P=0.135). Among the evaluated parameters, only systolic blood pressure in AGA group was significantly higher than control group.Conclusion.In contrast to the most of the previous studies, our study does not support the link between AGA and MS. To exclude confounding factors such as advanced age and therefore metabolic disturbances, further studies are needed with large group of AGA patients including different age groups and varying severity.


1988 ◽  
Vol 69 (2) ◽  
pp. 234-238 ◽  
Author(s):  
Vidar Bosnes ◽  
Henry Hirschberg

✓ Peripheral blood mononuclear cells from 11 glioma patients and 11 healthy control subjects were cultured in medium containing recombinant interleukin-2 for a period of 5 days. The cytotoxicity of these lymphokine-activated killer (LAK) cells was tested on chromium-51-labeled freshly prepared allogeneic glioblastoma cells, and on the cell lines K562 (natural killer cell (NK)-sensitive) and Daudi (NK-resistant). Peripheral blood mononuclear cells from all subjects showed high levels of cytotoxicity against these targets. There was no significant difference between the patients and the control group when LAK cytotoxicity was compared. Thus, although glioma patients are known to have depressed immunological reactivity, the cytotoxic capacity of LAK cells derived from glioma patients is similar to that of LAK cells from healthy control subjects. However, the glioma patients had significantly reduced numbers of mononuclear cells in their peripheral blood, possibly due to steroid treatment. Therefore, the volume of blood required to generate the same number of LAK cells was approximately three times larger from the glioma patients than from control subjects.


Sign in / Sign up

Export Citation Format

Share Document