Denaturation of human plasma high-density lipoproteins by urea studied by apolipoprotein A-I dissociation

Dergunov, Alexander D.; Litvinov, Dmitry; Malkov, Artem A.; Baserova, V.B.; Nosova, Elena V.; Dergunova, Lyudmila V.

doi:10.1016/j.bbalip.2020.158814

Cited by 5 publications

(5 citation statements)

References 52 publications

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“…The immunoblotting results further demonstrated that the decreased protein expression of ABCA1 and ApoA1 was significantly restored after c-MSST ( Figures 3 H–3J). ABCA1 loaded the outflow of cholesterol and phospholipids from cells to lipid-poor apolipoproteins (ApoA1 and ApoE), thus generating nascent high-density lipoproteins ( Dergunov et al., 2021 ). A significant increase in cholesterol intensity might disrupt synaptic plasticity and lead to cognitive impairment ( Loera-Valencia et al., 2021 ).…”

Section: Resultsmentioning

confidence: 99%

“…Because cells in the CNS do not produce ApoA1, brain cells must acquire a significant amount of ApoA1 from the blood to maintain their functions via unknown mechanisms ( Koch et al., 2001 ; Stukas et al., 2014 ). ABCA1 loaded the out flow of cholesterol and phospholipids from cells to lipid-poor apolipoproteins (ApoA1 and ApoE), thus generating nascent high-density lipoproteins ( Dergunov et al., 2021 ). Moreover, disordered lipid metabolism because of dysregulated cholesterol efflux may be involved in depression-induced cognitive disorders ( Ye et al., 2020 ).…”

Section: Discussionmentioning

confidence: 99%

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Selective activation of ABCA1/ApoA1 signaling in the V1 by magnetoelectric stimulation ameliorates depression via regulation of synaptic plasticity

Jiao

et al. 2022

iScience

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Selective activation of ABCA1/ApoA1 signaling in the V1 by magnetoelectric stimulation ameliorates depression via regulation of synaptic plasticity

Jiao

et al. 2022

iScience

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“…However, we previously showed that hepatic Abca1 expression is not altered in Abcc6 −/− mice 36 . A recent study by Dergunov et al 2020 showed that increased ApoA-I serum levels might be associated with higher ApoA-I release of HDL particles 37 . Released ApoA-I determines the increase of cholesterol efflux of macrophages to circulating HDL.…”

Section: Discussionmentioning

confidence: 99%

Genetic deletion of Abcc6 disturbs cholesterol homeostasis in mice

Ibold

Tiemann

Faust

et al. 2021

Sci Rep

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Genetic studies link adenosine triphosphate-binding cassette transporter C6 (ABCC6) mutations to pseudoxanthoma elasticum (PXE). ABCC6 sequence variations are correlated with altered HDL cholesterol levels and an elevated risk of coronary artery diseases. However, the role of ABCC6 in cholesterol homeostasis is not widely known. Here, we report reduced serum cholesterol and phytosterol levels in Abcc6-deficient mice, indicating an impaired sterol absorption. Ratios of cholesterol precursors to cholesterol were increased, confirmed by upregulation of hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase (Hmgcr) expression, suggesting activation of cholesterol biosynthesis in Abcc6−/− mice. We found that cholesterol depletion was accompanied by a substantial decrease in HDL cholesterol mediated by lowered ApoA-I and ApoA-II protein levels and not by inhibited lecithin-cholesterol transferase activity. Additionally, higher proprotein convertase subtilisin/kexin type 9 (Pcsk9) serum levels in Abcc6−/− mice and PXE patients and elevated ApoB level in knockout mice were observed, suggesting a potentially altered very low-density lipoprotein synthesis. Our results underline the role of Abcc6 in cholesterol homeostasis and indicate impaired cholesterol metabolism as an important pathomechanism involved in PXE manifestation.

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“…In view of the writing [21][22][23], the accompanying covariates were incorporated: age, race (Mexican American, Other Hispanic, Non-Hispanic White, Non-Hispanic Dark, and Other Race), BMI (underweight: less than 18.5 kg/m2; normal: ranging from 18.5 to 25 kg/m2; overweight: somewhere in the range of 25 and 30 kg/m2; obesity: over 30 kg/m2) [20], low-thickness lipoprotein cholesterol (LDL-C), serum creatinine, serum uric corrosive (SUA) and fatty oils. A questionnaire that asked participants to self-report having been diagnosed with hypertension or diabetes by a doctor was used to collect the history of hypertension or diabetes.…”

Section: Study Variablesmentioning

confidence: 99%

Exploration of high-density lipoprotein cholesterol level and serum testosterone concentrations in adult males from NHANES, 2011----2016

Liu

2023

TNS

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Past explores have shown the expected linkage between high-thickness lipoprotein cholesterol (HDL-C) and testosterone fixations, yet the relationship is as yet hazy and questionable among the more extensive male populace in the U.S. The target of this review is to survey the relationship between HDL-C focuses and serum testosterone in U.S. grown-up guys. Information for this populace based study were from the Public Wellbeing and Sustenance Assessment Overview (NHANES) traversing 2011-2016. In the wake of barring grown-up guys matured under 18 years of age and without serum testosterone or HDL-C information, the example enveloped 7,804 male subjects. Contrasted and grown-ups introducing standard HDL-C levels, people with lessened HDL-C fixations displayed diminished testosterone levels (P<0.01). In the fundamental univariable direct relapse examination, factors including age, BMI, HDL, hemoglobin, creatinine and uric corrosive were seen to have an opposite relationship with serum testosterone levels. In the multivariate straight relapse examination, lessening serum testosterone related with decreased HDL-C focuses (assessed testosterone rate difference: 0.36% per mg/dL, P<0.01). In responsiveness examinations that prohibited anomaly or outrageous worth, HDL-C level was emphatically related with testosterone focuses. All in all, this cross-sectional review demonstrated a positive linkage between HDL-C levels and serum testosterone focuses in grown-up guys, and further largescale planned examinations are fundamental for approval of the causality between HDL-C and testosterone.

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Denaturation of human plasma high-density lipoproteins by urea studied by apolipoprotein A-I dissociation

Cited by 5 publications

References 52 publications

Selective activation of ABCA1/ApoA1 signaling in the V1 by magnetoelectric stimulation ameliorates depression via regulation of synaptic plasticity

Selective activation of ABCA1/ApoA1 signaling in the V1 by magnetoelectric stimulation ameliorates depression via regulation of synaptic plasticity

Genetic deletion of Abcc6 disturbs cholesterol homeostasis in mice

Exploration of high-density lipoprotein cholesterol level and serum testosterone concentrations in adult males from NHANES, 2011----2016

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