DNA synthesis and 3-hydroxy-3-methylglutaryl CoA reductase activity in PHA stimulated human lymphocytes: A comparative study of the inhibitory effects of some oxysterols with special reference to side chain hydroxylated derivatives

Defay, Roselyne; Astruc, M.; Roussillon, Samia; Descomps, Bernard; Paulet, A. Crastes de

doi:10.1016/0006-291x(82)91118-4

Cited by 53 publications

(9 citation statements)

References 23 publications

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“…Hydroxylation of sterols generates a powerful inhibition of reductase activity. Defay et al [ 17 ] found that hydroxylated vitamin D derivatives inhibited HMG-CoA reductase activity in lymphocytes stimulated with phytohemaglutinin. Experimental studies in various cell lines have shown that treatment with cholecalciferol (vitamin D3) and its metabolites (25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol, and24, 25- dihydroxycholecalciferol) inhibit cholesterol synthesis due to inhibition of the activity of HMG-CoA reductase, a key enzyme in cholesterol synthesis.…”

Section: Resultsmentioning

confidence: 99%

Vitamin D Levels and Lipid Response to Atorvastatin

Pérez‐Castrillón

Manteca

Vega

et al. 2010

International Journal of Endocrinology

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Adequate vitamin D levels are necessary for good vascular health. 1,25-dihydroxycholecalciferol activates CYP3A4, an enzyme of the cytochrome P450 system, which metabolizes atorvastatin to its main metabolites. The objective of this study was to evaluate the response of cholesterol and triglycerides to atorvastatin according to vitamin D levels. Sixty-three patients with acute myocardial infarction treated with low and high doses of atorvastatin were included. Levels of total cholesterol, triglycerides, HDL cholesterol, and LDL cholesterol were measured at baseline and at 12 months of follow-up. Baseline levels of 25-hydroxyvitamin D (25-OHD) were classified as deficient (<30 nmol/L), insufficient (30–50 nmol/L), and normal (>50 nmol/L). In patients with 25-OHD <30 nmol/L, there were no significant changes in levels of total cholesterol (173 ± 47 mg/dL versus 164 ± 51 mg/dL), triglycerides (151 ± 49 mg/dL versus 177 ± 94 mg/dL), and LDL cholesterol (111 ± 48 mg/dL versus 92 45 ± mg/dL); whereas patients with insufficient (30–50 nmol/L) and normal vitamin D (>50 nmol/L) had a good response to atorvastatin. We suggest that vitamin D concentrations >30 nmol/L may be required for atorvastatin to reduce lipid levels in patients with acute myocardial infarction.

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Section: Resultsmentioning

confidence: 99%

Vitamin D Levels and Lipid Response to Atorvastatin

Pérez‐Castrillón

Manteca

Vega

et al. 2010

International Journal of Endocrinology

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“…It was reported that cholesterol oxides can inhibit DNA synthesis in replicating cells (57,58). This could be part of the reason for the toxicity observed in neuroretinal cultures, which consisted of both neurons and glial cells.…”

Section: Discussionmentioning

confidence: 96%

“…The disturbance of intracellular cytoskeleton could lead to pathological findings in neurons and glial cells. Finally, cholesterol oxides are potent inhibitors of 3-hydroxy-3-methylglutaryl (HMG) CoA reductase, a key enzyme in the endogenous biosynthesis of cholesterol (57,58). It is possible that severe inhibition of cholesterol synthesis in the cells could contribute to ultimate cell death.…”

Section: Discussionmentioning

confidence: 99%

Toxicity of cholesterol oxides on cultured neuroretinal cells

Chang

Liu

1998

Current Eye Research

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“…A separate feedback mechanism appears to be provided by calcidiol (25(OH)D), which has been shown to inhibit the function of HMGCR [171]. In cultured human lymphocytes, it was shown that calcidiol (25(OH)D) inhibited HMGCR activity by 63% and 93% at concentrations of 5 and 25 ug/mL, respectively.…”

Section: Feedback From Vitamin D Metabolitesmentioning

confidence: 99%

The Interdependency and Co-Regulation of the Vitamin D and Cholesterol Metabolism

Warren

McAllister

Morgan

et al. 2021

Cells

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Vitamin D and cholesterol metabolism overlap significantly in the pathways that contribute to their biosynthesis. However, our understanding of their independent and co-regulation is limited. Cardiovascular disease is the leading cause of death globally and atherosclerosis, the pathology associated with elevated cholesterol, is the leading cause of cardiovascular disease. It is therefore important to understand vitamin D metabolism as a contributory factor. From the literature, we compile evidence of how these systems interact, relating the understanding of the molecular mechanisms involved to the results from observational studies. We also present the first systems biology pathway map of the joint cholesterol and vitamin D metabolisms made available using the Systems Biology Graphical Notation (SBGN) Markup Language (SBGNML). It is shown that the relationship between vitamin D supplementation, total cholesterol, and LDL-C status, and between latitude, vitamin D, and cholesterol status are consistent with our knowledge of molecular mechanisms. We also highlight the results that cannot be explained with our current knowledge of molecular mechanisms: (i) vitamin D supplementation mitigates the side-effects of statin therapy; (ii) statin therapy does not impact upon vitamin D status; and critically (iii) vitamin D supplementation does not improve cardiovascular outcomes, despite improving cardiovascular risk factors. For (iii), we present a hypothesis, based on observations in the literature, that describes how vitamin D regulates the balance between cellular and plasma cholesterol. Answering these questions will create significant opportunities for advancement in our understanding of cardiovascular health.

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DNA synthesis and 3-hydroxy-3-methylglutaryl CoA reductase activity in PHA stimulated human lymphocytes: A comparative study of the inhibitory effects of some oxysterols with special reference to side chain hydroxylated derivatives

Cited by 53 publications

References 23 publications

Vitamin D Levels and Lipid Response to Atorvastatin

Vitamin D Levels and Lipid Response to Atorvastatin

Toxicity of cholesterol oxides on cultured neuroretinal cells

The Interdependency and Co-Regulation of the Vitamin D and Cholesterol Metabolism

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