scholarly journals The Expression of Allele Changes in NLRP3 (rs35829419) and IL-1β (+3954) Gene Polymorphisms in Periodontitis and Coronary Artery Disease

Materials ◽  
2021 ◽  
Vol 14 (17) ◽  
pp. 5103
Author(s):  
Jaideep Mahendra ◽  
Abirami Nayaki Rao ◽  
Little Mahendra ◽  
Mohammed E. Sayed ◽  
Maryam H. Mugri ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Gene Polymorphisms ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Conventional Polymerase Chain Reaction ◽  
Demographic Variables ◽  
Subgingival Plaque ◽  
Blood Samples ◽  
Artery Disease

Background: Inflammasomes have been shown to play a pivotal role in periodontal disease pathogenesis. However, their role in periodontitis subjects with coronary heart disease remains unclear. This study aimed to obtain the expression of NLRP3 (rs35829419) and IL-1β (+3954) gene polymorphisms in the subgingival plaque and blood samples of generalized periodontitis (GP) subjects with and without coronary heart disease (CHD). Methods: A total of 70 subjects were grouped into two; GP and GP with CHD. Demographic variables and periodontal and cardiac parameters were recorded from both the groups. Subgingival plaque and blood samples were obtained from both the groups and were further subjected to the identification of NLRP3 (rs35829419) and IL-1β (+3954) expression and allele change using a conventional polymerase chain reaction (PCR) and gene sequencing (Sanger’s method). Results: Amongst the demographic variables, age and monthly income were statistically significant between the two groups. Plaque index (PI), clinical attachment level (CAL), high-density lipoprotein (HDL), and low density-lipoprotein (LDL) exhibited statistically significant levels between the two groups. The NLRP3 (rs35829419) and IL-1β (+3954) genes showed a statistically significant association with allele change (frequency) among the groups. The general comparison of all the parameters with the allele change of NLRP3 (rs35829419) and IL-1β (+3954) in the subgingival plaque and blood samples showed statistically significant associations among the two groups. Conclusion: The present study highlighted an allele change in IL-1β (+3954) gene polymorphisms which may play an important role in the pathogenesis of periodontitis and coronary heart disease.

scholarly journals Genetic Polymorphisms of NLRP3 (rs4612666) and CARD8 (rs2043211) in Periodontitis and Cardiovascular Diseases

Biology ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 592
Author(s):  
Jaideep Mahendra ◽  
Abirami Nayaki Rao ◽  
Little Mahendra ◽  
Hytham N. Fageeh ◽  
Hammam Ibrahim Fageeh ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Conventional Polymerase Chain Reaction ◽  
Demographic Variables ◽  
Clinical Attachment Level ◽  
Significant Relationships ◽  
Polymerase Chain ◽  
Attachment Level

Background: The existing data show that inflammasomes play a role in periodontal disease pathogenesis. However, their role in the pathogenesis of periodontitis and coronary heart disease remains unclear. This study had the objective of assessing NLRP3 (rs4612666) and CARD8 (rs2043211) gene polymorphisms in dental plaque and blood of generalized chronic periodontitis (CP) patients in the presence and absence of coronary heart disease (CHD). Methods: A total of 70 subjects were divided into two groups, including CP and CP + CHD subjects. Demographic variables, periodontal, and cardiac parameters were recorded from both groups. Subgingival plaque and blood samples were obtained from both groups and were subjected to further molecular analysis for NLRP3 (rs4612666) and CARD8 (rs2043211) expression and allele change using conventional polymerase chain reaction (PCR) and gene sequencing (Sanger’s method). Results: Amongst the demographic variables, age, and monthly income were statistically significant between the two groups. Plaque index (PI), clinical attachment level (CAL), high-density lipoprotein (HDL), and low density-lipoprotein (LDL) exhibited statistically significant levels between the two groups. NLRP3 (rs4612666) and CARD8 (rs2043211) genes showed a statistically significant association of allele change (frequency) among the groups. In general, when all of the parameters were compared to the allele change of the genes, statistically significant relationships were found between the two groups. Conclusions: The present study expressed an allele change of the investigated genes which could profoundly affect the pathobiology of the two diseases under investigation.

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 The Description of Low Density Lipoprotein (LDL) Levels on Smoker and Non Smoker Adolescent in Buyan Hamlet, Pancasari Village, Sukasada District, Buleleng, Bali

2017 ◽  
Vol 4 (1) ◽  
pp. 39-44
Author(s):  
Ni Made Restina Juliani ◽  
I Putu Oka Dharmawan ◽  
Putu Ayu Parwati
Keyword(s):  
Physical Activity ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Ldl Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
The Body ◽  
Low Density ◽  
Blood Samples ◽  
Cholesterol Levels

Introduction: Low Density Lipoprotein (LDL) is a type of low-density lipoprotein and the most widely transported cholesterol in the body. Increased levels of LDL in the body can be affected by genetics, age, gender, obesity, physical activity, lifestyle, drug consumption and smoking. Substances in a cigarette can cause an increase of LDL levels. Increased of LDL cholesterol levels can cause Coronary Heart Disease (CHD). The purpose of this research is to know the description of Low Density Lipoprotein (LDL) levels on smoker and non-smoker adolescent in Buyan Hamlet, Pancasari Village, Sukasada District, Buleleng Bali. Method: The type of this research is descriptive. This research was conducted in April-May 2017, which used fasting blood samples of 42 respondents. Result: From the average result of LDL level in smoker adolescent that is 134,91 mg/dL higher than the average of LDL level in non-smoker adolescent that is 74,90 mg/dL. The result of LDL cholesterol levels was determined by 21 smoker adolescent respondents with the close to optimal category (100-129 mg/dL) as many as 9 people (42,8%), and 12 people (57,3%) with worry category (130-159 mg/dL). Whereas in 21 non-smoker adolescent respondents obtained  result of LDL cholesterol level test with optimal category (<100 mg/dL) counted 18 people (87,71%) and 3 person (14,30%) with close to optimal category (100-129 mg/dL). Discussion: Based on the results of this research can be concluded that in smoker adolescent obtained LDL levels with close to optimal category and worrying whereas in non-smoker adolescents obtained LDL levels in the optimal category and close to optimal.

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&gt; 2, p &lt; 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.

Isolation of plasma small-dense low-density lipoprotein using a simple air-driven ultracentrifuge and quantification using immunassay of apolipoprotein B

2004 ◽  
Vol 42 (1) ◽  
Author(s):  
Valentine C. Menys ◽  
Yifen Liu ◽  
Michael I. Mackness ◽  
See Kwok ◽  
Muriel J. Caslake ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Coronary Heart Disease Risk ◽  
Apolipoprotein B ◽  
Disease Risk ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Heart Disease Risk

AbstractSmall-dense low-density lipoprotein (SD-LDL) is associated with coronary heart disease risk. Current methods for its quantification are expensive, complex and time-consuming. Plasma was adjusted to a density (D) of 1.044 g/ml in a volume of 0.18 ml and centrifuged in a Beckman Airfuge at 160 000×

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