scholarly journals Peripheral Blood Mononuclear Phagocyte Subpopulations as Cellular Markers in Hypercholesterolemia

1996 ◽  
Vol 16 (12) ◽  
pp. 1437-1447 ◽  
Author(s):  
Gregor Rothe ◽  
Holger Gabriel ◽  
Eva Kovacs ◽  
Jochen Klucken ◽  
Josef Stöhr ◽  
...  
Keyword(s):  
Peripheral Blood ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Normal Subjects ◽  
Mononuclear Phagocyte ◽  
Mononuclear Phagocytes ◽  
Vascular Lesions ◽  
Peripheral Blood Mononuclear ◽  
Monocyte Subpopulations ◽  
Cellular Markers

Mononuclear phagocytes play a major role in the development of vascular lesions in atherogenesis. The goal of our study was to characterize circulating blood monocyte subpopulations as potential cellular markers of systemic immunological abnormalities in hypercholesterolemia. In normal subjects, three-parameter immunophenotyping of whole blood revealed that 61.3±6.0% of monocytes showed “bright” expression of the lipopolysaccharide receptor (LPSR: CD14) and Fcγ receptor I (RI: CD64) without expression of Fcγ-RIII (CD16). Other monocyte subsets (populations 2, 3, 4, and 5) were characterized by the simultaneous expression of both Fcγ-R's (25.6±5.0%), isolated expression of Fcγ-RIII (9.4±1.7%), or high expression of CD33 (3.7±1.1%) with only dim expression of CD14, respectively. The smallest subset of monocytes (population 5: 2.1±0.8%) differed from the predominant population of CD14 bright CD64 + CD16 − monocytes by additional expression of neural cell adhesion molecule (N-CAM: CD56). In a group of hypercholesterolemic patients (n=19), high density lipoprotein cholesterol levels were negatively correlated to the population size of CD64 − CD16 + monocytes. In both healthy subjects (n=55) and hypercholesterolemic patients, the rare apolipoprotein E3/E4 and E4/E4 phenotypes were associated with a tendency toward a larger population of CD64 − CD16 + monocytes. Expression of the variant activation antigen CD45RA by peripheral blood mononuclear phagocytes showed a positive correlation to plasma levels of the atherogenic lipoproteins low density lipoprotein and lipoprotein(a). These data suggest that systemic abnormalities in mononuclear phagocyte subpopulations may play a role in the pathogenesis of atherosclerosis.

Abstract P249: Effects of Lifestyle Changes on Metabolism and Early Vascular Lesion in Healthy People

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Xu Fengcheng ◽  
Yu Chaoping ◽  
Liu Tianhu
Keyword(s):  
Healthy Lifestyle ◽  
Low Density Lipoprotein ◽  
Fasting Blood Glucose ◽  
Ankle Brachial Index ◽  
Density Lipoprotein ◽  
Vascular Lesion ◽  
Lifestyle Changes ◽  
Healthy People ◽  
Vascular Lesions ◽  
Before And After

Objective: Through propaganda and education on lifestyle change, we study the effects on metabolism and vascular lesions in healthy people. Methods: the healthy subjects that conform to the requirements, through propaganda and education on vascular health, through moderate exercise, proper control of starchy foods, low salt, low fat diet, reduce smoking and other lifestyle changes, compare changes in weight, renal function, fasting blood glucose, blood lipids and ankle brachial index (ABI), cardio ankle vascular index(CAVI) before and after lifestyle changes. Results: After lifestyle changed, the subjects’ body mass index [(23.13±3.18)kg/m 2 vs (22.67±3.36)kg/m 2 ], ABI[1.11±0.08 vs 1.09±0.09], CAVI[(7.14±1.13 ) vs (7. 01±1.18) ], serum creatinine[(84.31±22.41)umol/L vs (79.92±23.64)umol/L], blood uric acid[(337.79±102.17 )umol/L vs (328.12±88.33)umol/L], low density lipoprotein cholesterol[(2.49±0.65) mmol/L vs (2.37±0.69) mmol/L],all have good changes. Conclusion: Healthy lifestyle is good for metabolism and early vascular lesions, can improve metabolic disorder and slow the occurrence of arteriosclerosis.

scholarly journals Abnormally expressed miR-23b in Chinese Mongolian at high cardiovascular risk may contribute to monocyte/macrophage inflammatory reaction in atherosclerosis

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Li-ping He ◽  
Xing-sheng Zhao ◽  
Le-ping He
Keyword(s):  
Cardiovascular Risk ◽  
Inflammatory Response ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Nuclear Factor Κb ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
High Cardiovascular Risk ◽  
Peripheral Blood Mononuclear

Background: The prevalence of coronary heart disease (CHD) appears to be high among Chinese Mongolians. MiR-23b has been proven to play a key role in atherosclerosis. The expression and role of miR-23b in the Mongolians at high cardiovascular risk were explored in the present study. Methods: Forty cases of blood samples from the Mongolians at high cardiovascular risk were enrolled in the present study. The expression of miR-23b was quantified by quantitative real-time PCR. To induce monocytes differentiation into macrophages, HP-1 cells were cultured with phorbol 12-myristate 13-acetate. The level of inflammatory markers was determined by the enzyme-linked immunosorbent assay. The interaction between miR-23b and A20 was explored by the dual luciferase reporter assay. Results: The expression of miR-23b in the Mongolian at high cardiovascular risk was higher than that in healthy Mongolian volunteers. Decrease in ATP-binding cassette transporter A1 caused by miR-23b is responsible for TC accumulation in the Mongolian at high cardiovascular risk. MiR-23b enhanced the oxidized low-density lipoprotein (oxLDL)-induced inflammatory response of THP-1 derived macrophage. MiR-23b regulated nuclear factor-κB (NF-κB) pathway through targeting A20. MiR-23b mediated oxLDL-induced inflammatory response of peripheral blood mononuclear cell in the Mongolian at high cardiovascular risk. Conclusion MiR-23b enhanced oxLDL-induced inflammatory response of macrophages in the Mongolian at high cardiovascular risk through the A20/NF-κB signaling pathway, and thus contributing to atherosclerosis.

scholarly journals Peripheral blood mononuclear phagocytes mediate dissemination of murine cytomegalovirus.

1994 ◽  
Vol 68 (10) ◽  
pp. 6243-6253 ◽  
Author(s):  
C A Stoddart ◽  
R D Cardin ◽  
J M Boname ◽  
W C Manning ◽  
G B Abenes ◽  
...  
Keyword(s):  
Peripheral Blood ◽  
Mononuclear Phagocytes ◽  
Murine Cytomegalovirus ◽  
Peripheral Blood Mononuclear

scholarly journals Knockdown of lncRNA ENST00000609755.1 Confers Protection Against Early oxLDL-Induced Coronary Heart Disease

2021 ◽  
Vol 8 ◽  
Author(s):  
Yi Sun ◽  
Shuna Huang ◽  
Chunyu Wan ◽  
Qishuang Ruan ◽  
Xiaoxu Xie ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Peripheral Blood ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Peripheral Blood Leukocyte ◽  
Loss Of Function ◽  
Human Coronary Artery ◽  
Injury Model

Background: This study investigated the association between long non-coding RNAs (lncRNAs) and coronary heart disease (CHD) and further elucidated the potential biological roles of lncRNAs in CHD pathogenesis.Methods: A case-control study (590 patients and 590 controls) was conducted from February 2017 and March 2019 in Fuzhou, China. Environmental factors were investigated using questionnaires and physical examinations. Five representative lncRNAs were screened using lncRNA microarray (peripheral blood in 5 cases and 5 controls) and further verified by quantitative real-time polymerase chain reaction (peripheral blood leukocyte in 100 cases and 100 controls). Oxidized low-density lipoprotein (oxLDL) was used to induce a human coronary artery endothelial cell (HCAECs) injury model, and loss of function was used to elucidate the role of lncRNA ENST00000609755.1 (lnc-MICALL2-2) in oxLDL-induced HCAECs injury.Results: A total of 320 lncRNAs were found dysregulated in CHD patients (fold change> 2, p < 0.05). The results of a discovery microarray, population verification and HCAEC experiments suggested the lnc-MICALL2-2 is upregulated in CHD subjects and in an oxLDL-induced HCAECs injury model. Conversely, lnc-MICALL2-2 inhibition in vitro attenuated the effects of oxLDL on HCAECs morphology, proliferation, and apoptosis.Conclusion: Elevated expression of lnc-MICALL2-2 is an independent risk factor for CHD, and knockdown subsequently confers protection against early pathological processes of oxLDL-induced CHD.

scholarly journals Statin-induced microRNAome alterations modulating inflammation pathways of peripheral blood mononuclear cells in patients with hypercholesterolemia

2020 ◽  
Vol 40 (9) ◽  
Author(s):  
Hung-Ju Lin ◽  
Sung-Liang Yu ◽  
Ta-Chen Su ◽  
Hsiu-Ching Hsu ◽  
Ming-Fong Chen ◽  
...  
Keyword(s):  
Peripheral Blood Mononuclear Cells ◽  
Immune Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Transforming Growth Factor ◽  
Quantitative Polymerase Chain Reaction ◽  
Density Lipoprotein ◽  
Cardiovascular Risks ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells

Abstract Statins inhibit cholesterol biogenesis and modulate atheroma inflammation to reduce cardiovascular risks. Promoted by immune and non-immune cells, serum C-reactive protein (CRP) might be a biomarker suboptimal to assess inflammation status. Although it has been reported that statins modulated inflammation via microRNAs (miRNAs), evidence remains lacking on comprehensive profiling of statin-induced miRNAome alterations in immune cells. We recruited 19 hypercholesterolemic patients receiving 2 mg/day pitavastatin and 15 ones receiving 10 mg/day atorvastatin treatment for 12 weeks, and performed microarray-based profiling of 1733 human mature miRNAs in peripheral blood mononuclear cells (PBMCs) before and after statin treatment. Differentially expressed miRNAs were determined if their fold changes were >1.50 or <0.67, after validated using quantitative polymerase chain reaction (qPCR). The miRSystem and miTALOS platforms were utilized for pathway analysis. Of the 34 patients aged 63.7 ± 6.2 years, 27 were male and 19 were with coronary artery disease. We discovered that statins induced differential expressions of miR-483-5p, miR-4667-5p, miR-1244, and miR-3609, with qPCR-validated fold changes of 1.74 (95% confidence interval, 1.33–2.15), 1.61 (1.25–1.98), 1.61 (1.01–2.21), and 1.68 (1.19–2.17), respectively. The fold changes of the four miRNAs were not correlated with changes of low-density-lipoprotein cholesterol or CRP, after sex, age, and statin type were adjusted. We also revealed that RhoA and transforming growth factor-β signaling pathways might be regulated by the four miRNAs. Given our findings, miRNAs might be involved in statin-induced inflammation modulation in PBMCs, providing likelihood to assess and reduce inflammation in patients with atherosclerotic cardiovascular diseases.

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