Low concentrations of phospholipids and plasma HDL cholesterol subclasses in asymptomatic subjects with high coronary calcium scores

García-Sánchez, Cynthia; Posadas‐Romero, Carlos; Posadas-Sánchez, Rosalinda; Carreón‐Torres, Elizabeth; Rodrı́guez-Pérez, José Manuel; Juárez-Rojas, Juan Gabriel; Martínez‐Sánchez, Carlos; Fragoso, José Manuel; González‐Pacheco, Héctor; Vargas‐Alarcón, Gilberto; Pérez-Méndez, Óscar

doi:10.1016/j.atherosclerosis.2014.12.004

Cited by 22 publications

(30 citation statements)

References 48 publications

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“…Furthermore, the relative proportions of each HDL subclass were expressed as the percentage of the total HDL protein. The mean intra‐assay variation of the relative proportions of the five HDL subclasses was 6.9% and 5.6% for cholesterol and phospholipids, respectively, as previously reported (Garcia‐Sanchez et al, ; Huesca‐Gomez et al, ; Toledo‐Ibelles et al, ; Warnick et al, ).…”

Section: Methodssupporting

confidence: 84%

“…HDL particles were isolated via ultracentrifugation according to the procedure of Toledo‐Ibelles et al (). Further separation of HDL particles was performed according to their size by nondenaturing 3–30% polyacrylamide gradient gel electrophoresis as previously described (Garcia‐Sanchez et al, ; Huesca‐Gomez et al, ; Toledo‐Ibelles et al, ; Warnick et al, ). Briefly, HDL gels were stained for cholesterol using a mixture of cholesterol esterase, cholesterol oxidase, and peroxidase in 150 mM NaCl, 8.6 mM Na 2 HPO 4 , and 1.4 mM NaH 2 PO 4 buffer (PBS), pH 7.4 (Toledo‐Ibelles et al, ).…”

Section: Methodsmentioning

confidence: 99%

“…Gels were stained for total cholesterol using enzymatic mixtures (Garcia‐Sanchez et al, ; Toledo‐Ibelles et al, ). The electrophoresis gels were then scanned in a GS‐670 BioRad densitometer, destained, and stained again for proteins with Coomassie R‐250, before a second scan.…”

Section: Methodsmentioning

confidence: 99%

“…Cholesterol level of HDL subclasses was expressed as plasma concentration (mg/dL), estimated from the densitometric analysis, and the HDL‐C plasma concentration (Toledo‐Ibelles et al, ). We considered the size intervals as follows: HDL3c, 7.94–8.45 nm; HDL3b, 8.45–8.98 nm; HDL3a, 8.98–9.94 nm; HDL2a, 9.94–10.58 nm; and HDL2b, 10.58–13.59 nm (Garcia‐Sanchez et al, ; Toledo‐Ibelles et al, ).…”

Section: Methodsmentioning

confidence: 99%

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CETP and LCAT Gene Polymorphisms Are Associated with High‐Density Lipoprotein Subclasses and Acute Coronary Syndrome

Vargas‐Alarcón

Pérez-Méndez

Herrera‐Maya

et al. 2018

Lipids

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We evaluated whether CETP and LCAT gene polymorphisms are statistically associated with the high-density lipoprotein (HDL) size distribution, the cholesterol level of HDL subclasses, and the acute coronary syndrome (ACS) susceptibility. Two CETP gene polymorphisms (rs4783961 and rs708272) and one LCAT polymorphism (rs2292318) were genotyped by 5' exonuclease TaqMan assays in 619 patients with ACS and 607 control individuals. For HDL analysis, a subgroup of 100 healthy individuals was recruited; the HDL subclasses were separated via ultracentrifugation and polyacrylamide gradient gel electrophoresis under native conditions. Under a dominant model, the G allele of the rs708272 polymorphism was associated with an increased risk of ACS (odds ratios [OR] = 1.45, corrected p-value [pC ] = 0.036). The linkage disequilibrium analysis showed that one of the eight possible combinations was associated with the risk of developing ACS (OR = 1.52, pC = 0.02), which suggests that it may contribute to coronary atherosclerosis. The rs708272 G allele carriers had a lower concentration of cholesterol associated with the HDL2a and HDL3a subclasses when compared with subjects carrying the A allele. Carriers of LCAT rs2292318 A allele showed a lower concentration of high-density lipoprotein-cholesterol (HDL-C) in comparison to the GG genotype; the cholesterol associated with the each one of the five HDL subclasses was significantly lower in rs2292318 A than in GG subjects. In summary, this study demonstrates that the rs708272 polymorphism is associated with a heightened risk of developing ACS. In addition, we report the association of the rs708272 and rs2292318 polymorphisms with HDL-C levels and HDL subclasses.

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Section: Methodssupporting

confidence: 84%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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CETP and LCAT Gene Polymorphisms Are Associated with High‐Density Lipoprotein Subclasses and Acute Coronary Syndrome

Vargas‐Alarcón

Pérez-Méndez

Herrera‐Maya

et al. 2018

Lipids

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“…Moreover, when pathologies such as diabetes mellitus, dyslipidemia, hypertension, and chronic kidney disease (CKD) are present, the mechanisms that inhibit the deposition hydroxyapatite crystals at the vascular level are prone to be affected. [34] Therefore, in the last 20 years, the perception of vascular calcification as a pathology evoked by a passive consequence of aging has changed to the concept of an active phenomenon, in which hemodynamical, pathological, anatomical, genetic, and epigenetic factors interact to facilitate calcium deposition at the vascular level. [5]…”

Section: Introductionmentioning

confidence: 99%

Vascular Calcification

Pérez-Hernández

Aptilon-Duque

Blachman‐Braun

et al. 2017

Chinese Medical Journal

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Objective:Vascular calcification is the consequence of the complex interaction between genetic, environmental, and vascular factors, which ultimately lead to the deposition of calcium in the tunica intima (atherosclerotic calcification) or tunica media (Mönckenberg's sclerosis). Vascular calcification is also closely related to other pathologies, such as diabetes mellitus, dyslipidemia, and chronic kidney disease. It has been concluded that the degree of vascular calcification may vary from person to person, even if the associated pathologies and environmental factors are the same. Therefore, this suggests an important genetic contribution to the development of vascular calcification. This review aimed to find the most recent evidence about vascular calcification pathophysiology regarding the genetic aspects and molecular pathways.Data Sources:We conducted an exhaustive search in Scopus, EBSCO, and PubMed with the keywords “genetics and vascular calcification”, “molecular pathways, genetic and vascular calcification” and included the main articles from January 1995 up to August 2016. We focused on the most recent evidence about vascular calcification pathophysiology regarding the genetic aspects and molecular pathways.Study Selection:The most valuable published original and review articles related to our objective were selected.Results:Vascular calcification is a multifactorial disease; thus, its pathophysiology cannot be explained by a single specific factor, rather than by the result of the association of several genetic variants, molecular pathway interactions, and environmental factors that promote its development.Conclusion:Although several molecular aspects of this mechanism have been elucidated, there is still a need for a better understanding of the factors that predispose to this disease.

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Epicardial Adipose Tissue in the Progression and Calcification of the Coronary Artery Disease

Luna-Luna

Zentella‐Dehesa²,

Pérez-Méndez

2020

Biochemistry of Cardiovascular Dysfunction in Obesity

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Low concentrations of phospholipids and plasma HDL cholesterol subclasses in asymptomatic subjects with high coronary calcium scores

Cited by 22 publications

References 48 publications

CETP and LCAT Gene Polymorphisms Are Associated with High‐Density Lipoprotein Subclasses and Acute Coronary Syndrome

CETP and LCAT Gene Polymorphisms Are Associated with High‐Density Lipoprotein Subclasses and Acute Coronary Syndrome

Vascular Calcification

Epicardial Adipose Tissue in the Progression and Calcification of the Coronary Artery Disease

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