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Authors: Zingg, Jean‐Marc | Ricciarelli, Roberta | Azzi, Angelo

Article Type: Research Article

Abstract: Atherosclerosis and its complications, such as coronary heart disease, heart infarction and stroke, are the leading causes of death in the developed world. High blood pressure, diabetes, smoking and a diet high in cholesterol and lipids clearly increase the likelihood of premature atherosclerosis, albeit other factors, such as the individual genetic makeup, may play an additional role. During atherosclerosis, uncontrolled cholesterol and lipid accumulation in macrophages and smooth muscle cells leads to foam cell formation and to the progression of the atherosclerotic plaque. This review will focus on foam cell formation within the atherosclerotic lesion, the involvement of the scavenger …receptor genes in this process, and the possibility to interfere with scavenger receptor function to reduce the progression of atherosclerosis. To date, the regulatory mechanisms for the expression of scavenger receptor genes and their role in atherosclerosis are not well characterized. Knowledge on this subject could lead to a better understanding of the process, prevention and therapy of this disease. Show more

Keywords: Scavenger receptors, atherosclerosis, gene expression

Citation: Biofactors, vol. 11, no. 3, pp. 189-200, 2000

Authors: Azzi, Angelo | Aratri, Elisabetta | Boscoboinik, Daniel | Clément, Sophie | Özer, Nesrin K. | Ricciarelli, Roberta | Spycher, Stefan

Article Type: Research Article

Abstract: Rat and human vascular smooth muscle cell proliferation is specifically sensitive to \alpha ‐tocopherol, but not \beta ‐tocopherol. The former, but not the latter, is capable of limiting proliferation and inhibiting protein kinase C activity in a dose‐dependent manner. The phenomenon occurs at concentrations in the range 10–50 \mu M. \beta ‐tocopherol addition together with \alpha ‐tocopherol, prevents both cell growth and protein kinase C inhibition. \alpha ‐tocopherol increases de novo synthesis of protein kinase C molecules. The enzyme specific activity, however, is diminished, due to a decreased phosphorylation of protein kinase C, occurring in the presence of \alpha ‐tocopherol. …Experiments with protein kinase C isoform‐specific inhibitors and precipitating antibodies show that the only isoform affected by \alpha ‐tocopherol is protein kinase C‐\alpha . The effect of \alpha ‐tocopherol is prevented by okadaic acid indicating a phosphatase of the PP2A type as responsible for protein kinase C‐\alpha dephosphorylation produced in the presence of \alpha ‐tocopherol. At a gene level \alpha ‐tocopherol but not \beta ‐tocopherol induces a transient activation of \alpha ‐tropomyosin gene transcription and protein expression. It is proposed that, by inhibiting protein kinase C activity via an activation of a phosphatase PP2A, \alpha ‐tocopherol controls smooth muscle cell proliferation through changes in gene expression. Show more

Keywords: \alpha‐tocopherol, vitamin E, protein kinase C, vascular smooth muscle cell, cell proliferation, protein phosphatase, oxidative stress

Citation: Biofactors, vol. 7, no. 1-2, pp. 3-14, 1998

Authors: Canepa, Elisa | Borghi, Roberta | Viña, Jose | Traverso, Nicola | Gambini, Juan | Domenicotti, Cinzia | Marinari, Umberto M. | Poli, Giuseppe | Pronzato, Maria A. | Ricciarelli, Roberta

Article Type: Research Article

Abstract: Accumulating data supports the concept that alterations of cholesterol metabolism might influence the development of Alzheimer's disease (AD), a neurodegenerative disorder characterized by progressive accumulation of amyloid-β (Aβ) peptides in the brain. Changes in the neuronal production of Aβ have been described as a function of cholesterol levels, thus suggesting a causal link between cholesterol homeostasis dysregulation and AD pathogenesis. Under physiological conditions, cholesterol uptake in the brain is efficiently prevented by the blood-brain barrier, and mature neurons are thought to rely on glial cells for their cholesterol supply. In the present study, we tested the hypothesis that Aβ may …serve as a signaling molecule capable of informing the astroglial network about the neuronal need for cholesterol. Collectively, our data bolster this hypothesis and demonstrate, for the first time, that Aβ42 exerts an inhibitory effect on the expression of the cholesterol transporter ABCA1 in cultured astrocytes. Accordingly, we also show that ABCA1 expression is reduced in the brain of AβPP/PS1 transgenic mice. These results provide a biological function for Aβ peptides and may help to define the pathogenic relationship between cholesterol metabolism in brain and AD. Show more

Keywords: Alzheimer's disease, amyloid-β protein precursor, ATP-binding cassette transporter A1, sterols

DOI: 10.3233/JAD-2011-110053

Citation: Journal of Alzheimer's Disease, vol. 25, no. 4, pp. 645-653, 2011