Vitamin A: a drug for prevention of restenosis/reocclusion after percutaneous coronary intervention?

Gidlöf, Anders; Ocaya, Pauline; Krivospitskaya, Olesya; Sirsjö, Allan

doi:10.1042/cs20070090

Cited by 12 publications

(13 citation statements)

References 79 publications

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“…This is plausible since retinoic acid, the bioactive form of vitamin A, regulates genes expression concerning cellular growth, differentiation and apoptosis, has antioxidative properties, participates in angiogenesis and reactivity of endothelial and smooth muscle cells, modulates cell interactions in inflammation [1][2][3][4][5][6][7], and can impair arterial re-stenosis [3,5].…”

Section: Introductionmentioning

confidence: 99%

Low plasma retinol predicts coronary events in healthy middle-aged men: The PRIME Study

et al. 2010

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a b s t r a c tThe role of plasma retinol and carotenoids in coronary heart disease (CHD) remains unclear. The PRIME Study prospectively evaluated these in France and Northern Ireland in 9758 men aged 50-59 years who were free of CHD at baseline. After five years' follow-up 150 incident cases of CHD (non-fatal myocardial infarction and fatal CHD) were compared with 285 controls matched for age, date of blood collection and study centre. Geometric means of major carotenoids did not differ significantly between cases and controls (P > 0.05), whereas the absolute and lipid-standardized plasma retinol levels were 9% lower in cases than controls in both countries (P < 0.002), without correlation with carotenoids. After adjusting for risk factors, the relative risks (RRs) of CHD in the first four quintiles of retinol distribution in controls (≤601, −683, −760, and −846 g/l) were 2.65 (P = 0.0009), 1.70, 1.03, and 1.12 (all P > 0.05) respectively, relative to the top quintile (retinol ≥846 g/l; linear trend P = 0.0001). The 10th percentile of lipid-standardized retinol (≤544 g/l) predicted an RR of 4.7 (P < 0.001). The risk associated with low retinol was comparable to strong risk factors (e.g. HDL-cholesterol, Interleukin-6) and behaved additively.In conclusion, plasma retinol levels of <601 g/l in a fifth of middle-aged European men place them at an approximately threefold RR of developing CHD. Thus the intake of vitamin A might be too low in middle-aged men. These findings must be confirmed.

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Section: Introductionmentioning

confidence: 99%

Low plasma retinol predicts coronary events in healthy middle-aged men: The PRIME Study

et al. 2010

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“…Therapeutic targeting of local retinoid turnover to increase local retinoid levels is an alternative strategy (2), and inhibitors of cytochrome P450, family 26 (CYP26) enzymes have been used in clinical studies (16,17). However, knowledge about the metabolism of atRA and other RAR ligands in atherosclerosis has been lacking.…”

Section: Introductionmentioning

confidence: 99%

“…For example, activation of retinoic acid receptors (RARs) reduces inflammation, vascular cell proliferation and migration, apoptosis, coagulation and matrix remodeling (2)(3)(4)(5), and retinoic acid upregulates a set of antiatherogenic genes in macrophages (6). Furthermore, retinoic acid promotes differentiation of regulatory T cells, an immune cell subset that ameliorates inflammation and atherosclerosis (1,7,8).…”

Section: Introductionmentioning

confidence: 99%

A CYP26B1 Polymorphism Enhances Retinoic Acid Catabolism and May Aggravate Atherosclerosis

Krivospitskaya

Elmabsout

Sundman

et al. 2012

Mol Med

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All-trans retinoic acid, controlled by cytochrome P450, family 26 (CYP26) enzymes, potentially has beneficial effects in atherosclerosis treatment. This study investigates CYP26 subfamily B, polypeptide 1 (CYP26B1) in atherosclerosis and the effects of a genetic polymorphism in CYP26B1 on retinoid catabolism. We found that CYP26B1 mRNA was induced by retinoic acid in human atherosclerotic arteries, and CYP26B1 and the macrophage marker CD68 were colocalized in human atherosclerotic lesions. In mice, Cyp26B1 mRNA was higher in atherosclerotic arteries than in normal arteries. Databases were queried for nonsynonymous CYP26B1 single nucleotide polymorphisms (SNPs) and rs2241057 selected for further studies. Constructs of the CYP26B1 variants were created and used for production of purified proteins and transfection of macrophagelike cells. The minor variant catabolized retinoic acid with significantly higher efficiency, indicating that rs2241057 is functional and suggesting reduced retinoid availability in tissues with the minor variant. rs2241057 was investigated in a Stockholm Coronary Atherosclerosis Risk Factor (SCARF) subgroup. The minor allele was associated with slightly larger lesions, as determined by angiography. In summary, this study identifies the first CYP26B1 polymorphism that alters CYP26B1 capacity to metabolize retinoic acid. CYP26B1 was expressed in macrophage-rich areas of human atherosclerotic lesions, induced by retinoic acid and increased in murine atherosclerosis. Taken together, the results indicate that CYP26B1 capacity is genetically regulated and suggest that local CYP26B1 activity may influence atherosclerosis.

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“…However, this protective role of endothelial cells is no longer evident in patients following exposure to stents, and they become more prone to a number of risk factors that cause the narrowing of the vascular lumen [17, 18]. Some review articles suggest that administration of drugs and vitamins, either orally or intravenously, is essential to prevent restenosis and in-stent restenosis [19–21]. Although this therapeutic strategy has been previously tested, it has not been shown to be consistently helpful.…”

Section: Discussionmentioning

confidence: 99%

Bo-Gan-Whan regulates proliferation and migration of vascular smooth muscle cells

Lee

Kim

et al. 2016

BMC Complement Altern Med

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BackgroundBo-Gan-Whan (BGH), a Korean polyherbal medicine, is used as a hepatoprotective drug. It has six natural sources, and has been demonstrated to have anti-oxidative, anti-cancer, and anti-inflammatory properties; however, its effect on vascular diseases remains unclear.MethodsCell viability and proliferation assays were employed using an EZ-Cytox Cell Viability Assay Kit. Platelet-derived growth factor (PDGF)-BB-induced vascular smooth muscle cell (VSMC) migration was measured by scratch wound healing assay and Boyden chamber assay. The expression levels of the phosphorylated signaling proteins relevant to proliferation, including extracellular signal-regulated kinase (ERK) 1/2 and p38 mitogen-activated protein kinase (MAPK) were determined by western blot analysis. Chromatogram and mass analysis were employed by Ultra Performance Liquid Chromatography (UPLC) system. Cell prolife ration and migration were also explored using the PDGF-BB-induced aortic sprout assay.ResultsBGH (100–500 μg/mL) significantly inhibited the proliferation and migration of PDGF-BB-stimulated VSMCs through the reduced phosphorylation of ERK1/2 and p38 MAPK in comparison to untreated PDGF-BB-stimulated VSMC. Moreover, we identified the paeoniflorin as the major composition of BGH.ConclusionsWe suggest that BGH may have an anti-atherosclerosis effect by inhibiting the proliferation and migration of PDGF-BB-stimulated VSMCs through down-regulation of ERK1/2 and p38 MAPK phosphorylation.

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Vitamin A: a drug for prevention of restenosis/reocclusion after percutaneous coronary intervention?

Cited by 12 publications

References 79 publications

Low plasma retinol predicts coronary events in healthy middle-aged men: The PRIME Study

Low plasma retinol predicts coronary events in healthy middle-aged men: The PRIME Study

A CYP26B1 Polymorphism Enhances Retinoic Acid Catabolism and May Aggravate Atherosclerosis

Bo-Gan-Whan regulates proliferation and migration of vascular smooth muscle cells

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