scholarly journals Scavenger Receptor BI Induced by HDL From Coronary Heart Disease May Be Related to Atherosclerosis

2021 ◽  
Vol 27 ◽  
pp. 107602962110297
Author(s):  
Fen Gao ◽  
Gao-jie Feng ◽  
Hong Li ◽  
Wei-wei Qin ◽  
Chuan-shi Xiao
Keyword(s):  
Myocardial Infarction ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Lipid Accumulation ◽  
Scavenger Receptor ◽  
Density Lipoprotein ◽  
Expression Levels ◽  
Class B ◽  
Dysfunctional Hdl

This study aims to determine whether dysfunctional High Density Lipoprotein (HDL) influenced the expression of scavenger receptor class B type Ⅰ (SR-B1) to determine reverse cholesterol transport. Blood samples obtained from coronary heart disease patients confirmed by angiography were collected. HDL was extracted from the blood via ultracentrifugation. Then, the HDL was injected into apoE−/− mice, and the HepG2 cells cultured with Dulbecco’s modified eagle medium (DMEM) were added the HDL extracted from coronary heart disease patients. As controls, normal cases without coronary heart disease (CHD) and patients with angina pectoris and acute myocardial infarction were used. The protein expression levels of SR-B1 were detected by western blot, and the lipid accumulation levels were detected by Oil Red O staining in both tissues and cell levels. These results revealed that the HDL obtained from CHD patients downregulate the SR-B1 expression in ex vitro and in vitro studies. In addition, dysfunctional HDL may result in lower SR-B1 expression levels. The degree of SR-B1 expression levels could be relative to the degree of coronary congestion. Along with the increase in severe coronary congestion, such as myocardial infarction, the SR-B1 expression levels were lower. The dysfunctional HDL derived from coronary heart disease patients decreased the expression of SR-B1, and promoted lipid accumulation.

scholarly journals Investigation of Scavenger Receptor Class B Type I gene variants in patients with coronary heart disease with a history of early myocardial infarction

2021 ◽  
Vol 49 (8) ◽  
pp. 641-653
Author(s):  
Burcu Çaykara ◽  
◽  
Bengü Tokat ◽  
Ender Coşkunpınar ◽  
Özlem Küçükhüseyin ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Scavenger Receptor ◽  
Type I ◽  
Gene Variants ◽  
Scavenger Receptor Class ◽  
Class B ◽  
History Of ◽  
I Gene

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.

Association of apolipoprotein E polymorphism, low-density lipoprotein cholesterol, and coronary artery disease.

1986 ◽  
Vol 32 (5) ◽  
pp. 778-781 ◽  
Author(s):  
H J Lenzen ◽  
G Assmann ◽  
R Buchwalsky ◽  
H Schulte
Keyword(s):  
Myocardial Infarction ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Apolipoprotein E ◽  
Ldl Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Apolipoprotein E Polymorphism ◽  
Artery Disease

Abstract We determined the frequencies of genetic apolipoprotein E isoforms in 570 survivors of myocardial infarction, all with demonstrable coronary heart disease, as compared with 624 healthy persons. In controls, E-4/E-3 heterozygosity was associated with total cholesterol concentrations of 1985 (SD 364) mg/L and low-density lipoprotein (LDL)-cholesterol concentrations of 1306 (SD 332) mg/L. Significantly lower values, 1811 (SD 312) mg/L and 1121 (SD 274) mg/L, respectively, were observed for E-3/E-2 heterozygous persons. In survivors of myocardial infarction, the respective values were significantly higher than in controls, differing between E-4/E-3 and E-3/E-2 heterozygous patients by 233 and 220 mg/L, respectively. Moreover, E-4/E-3 heterozygosity was accompanied by earlier age of myocardial infarction (48.8 +/- 7.4 years) as compared with E-3/E-2 heterozygosity (53.4 +/- 6.9 years) and E-3/E-3 homozygosity (51.2 +/- 7.7 years). Evidently, apolipoprotein E polymorphism can contribute to total and LDL-cholesterol concentrations in serum, thereby affecting risk of coronary heart disease and myocardial infarction.

scholarly journals Scavenger Receptor Class B Type I Is More Conducive to Hepatitis C Virus Invasion Compared with Low-Density Lipoprotein Receptor

2020 ◽  
Author(s):  
Xiangyi Cao ◽  
Qiong Kang ◽  
Deng Jiang ◽  
Jun Xiao ◽  
Yanyu Zhang ◽  
...  
Keyword(s):  
Low Density Lipoprotein ◽  
Scavenger Receptor ◽  
Density Lipoprotein ◽  
Type I ◽  
Lipoprotein Receptor ◽  
Scavenger Receptor Class ◽  
Recombinant Cells ◽  
Class B ◽  
Density Lipoprotein Receptor

Abstract Background: Hepatitis C virus is the major cause of chronic hepatitis which may deteriorate into liver cirrhosis or hepatocellular carcinoma. A number of studies have demonstrated that HCV cell entry is a complex multi-step process involving several cellular proteins, such as scavenger receptor class B type I (SR-BI), tetraspanin CD81, tight junction protein claudin-1 (CLDN-1) and occludin (OCLN). The low-density lipoprotein receptor (LDLR) is an important factor during the initial HCV particle-binding step, which interacts with the complex formed between the virus particle and the lipoprotein in the blood. However, the process of HCV early infection is not well-established, with many details remaining to be elucidated.This research aimed to study the early entry stage of HCV virus particles and the role of LDLR more effectively.Methods: Recombinant murine cell models of HCV infection in vitro was constructed, that expressed human HCV receptors, such as LDLR, CD81, SR BI, CLDN-1, and OCLN. These factors were also introduced to mice by hydrodynamic delivery to construct a humanized mouse model of HCV infection in vivo.Expression levels of the mRNA of HCV entry factors in recombinant cells were measured by qRT-PCR.Western blotting was used to determine whether the recombinant cells successfully expressed cellular proteins. HCV RNA was assayed by q-PCR following the incublation of HCVsd and HCVcc with the transgenice.Results: Transgenic murine cell lines and mice were developed successfully, and expressed four or five human HCV entry factors in tandem or individually, respectively. We found that all of these transgenic cells and mice were susceptible to HCV, and five entry factors (5EF) rendered higher infectivity. Additionally, we observed that four entry factors (4EF/hLDLR-) could facilitate abundant HCV entry, but four other factors (4EF/hSR-BI-) were less effective.Conclusions: Whether in vitro or in vivo, SR-BI is an essential factor in HCV invasion, and target cells and mice were more vulnerable to the virus in the presence of SR-BI than LDLR. These results suggested that SR-BI may be a potential drug target to inhibit HCV early infection, and the absence of LDLR could reduce the infectivity to the virus.

Effects of two lipid-lowering, carotenoid-controlled diets on the oxidative modification of low-density lipoproteins in free-living humans

2003 ◽  
Vol 105 (3) ◽  
pp. 355-361 ◽  
Author(s):  
Kiran D. K. AHUJA ◽  
Emma L. ASHTON ◽  
Madeleine J. BALL
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Dietary Intervention ◽  
Density Lipoprotein ◽  
Oxidative Modification ◽  
Lipid Lowering ◽  
Carotenoid Content ◽  
Lag Phase ◽  
Low Density

This study compares the effects of two lipid-lowering diets [a diet enriched in MUFAs (monounsaturated fatty acids) and a HCLF (high-carbohydrate/low-fat) diet] with a controlled carotenoid content on risk factors for coronary heart disease, including in vitro copper-induced LDL (low-density lipoprotein) oxidation and serum lipid levels. A randomized crossover dietary intervention study, with two diets each consumed for 14–16 days, was conducted in 18 women and 13 men aged 20–70 years, recruited via personal contacts and advertisements in newspapers. Both diets (MUFA-enriched diet and HCLF diet) contained the same basic foods and had a controlled carotenoid content, high in lycopene. The in vitro copper-induced oxidation of isolated LDL showed a longer lag phase (mean difference 7.4 min in women and 7.34 min in men) after the MUFA-enriched diet compared with the HCLF diet. Serum total cholesterol, LDL cholesterol and carotenoid levels were similar after the two diets. Serum triacylglycerol levels were significantly lower and those of HDL (high-density lipoprotein) cholesterol were significantly higher at the end of the MUFA-enriched diet compared with the HCLF diet. It is concluded that the significantly longer lag phase for oxidation of LDL, the higher HDL cholesterol level and the lower triacylglycerol level in subjects following a carotenoid-controlled, MUFA-enriched diet may decrease the risk of coronary heart disease.

scholarly journals Allelic Variants of the Human Scavenger Receptor Class B Type 1 and Paraoxonase 1 on Coronary Heart Disease

2005 ◽  
Vol 25 (4) ◽  
pp. 854-860 ◽  
Author(s):  
Francisco Rodríguez-Esparragón ◽  
José C. Rodríguez-Pérez ◽  
Yaridé Hernández-Trujillo ◽  
Antonio Macías-Reyes ◽  
Alfonso Medina ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Scavenger Receptor ◽  
Paraoxonase 1 ◽  
Allelic Variants ◽  
Scavenger Receptor Class ◽  
Class B

Primary risk factors influence risk of recurrent myocardial infarction/death from coronary heart disease: results from the Stockholm Heart Epidemiology Program (SHEEP)

2007 ◽  
Vol 14 (4) ◽  
pp. 532-537 ◽  
Author(s):  
Karin Leander ◽  
Björn Wiman ◽  
Johan Hallqvist ◽  
Tomas Andersson ◽  
Anders Ahlbom ◽  
...  
Keyword(s):  
Risk Factors ◽  
Myocardial Infarction ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Job Strain ◽  
Enzyme Level ◽  
Density Lipoprotein ◽  
Apolipoprotein A1 ◽  
Increased Risk

Background Prognosis after a first myocardial infarction (MI) is influenced by primary risk factors as well as secondary risk factors. There is still a lack of follow-up studies of well-characterized patient cohorts assessing the relative importance of these factors. Design A cohort of 1635 patients (aged 45-70 years) surviving at least 28 days after a first MI were followed for 6-9 years with regard to recurrent MI/fatal coronary heart disease (CHD). Data were collected through questionnaires, physical examinations, and medical records. Methods Hazard ratios (HR) with 95% confidence intervals (CI) for different risk factors were calculated using the Cox proportional hazard model. Results Of the primary risk factors, diabetes in both sexes was the most important predictor of recurrent MI/fatal CHD, multivariate-adjusted HR in men 1.6 (95% CI; 1.0-2.4) and in women 2.5 (95% CI; 0.9-6.9). Other primary risk factors with prognostic influence were job strain, HR 1.5 (95% CI; 1.0-2.1), and central obesity, HR 1.4 (95% CI; 1.0-2.0), in men and a low level of apolipoprotein A1, HR 2.3 (95% CI; 1.1-5.0), and high-density lipoprotein cholesterol, HR 1.9 (95% CI; 0.9-4.1), in women. The secondary risk factors most detrimental for prognosis were heart failure in men, HR 2.2 (95% CI; 1.2-4.0), and a high peak acute cardiac enzyme level in women, HR 4.4 (95% CI; 2.0-9.7). Conclusions Long-term follow-up of patients who survived at least 28 days after a first MI shows that several primary cardiovascular risk factors, particularly diabetes, contribute to the increased risk of recurrent MI/fatal CHD.

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