Cells exposed to simvastatin or to methyl-beta-cyclodextrin show reduced poliovirus infection, without alteration in virus binding or on the kinetics of genome entry, suggesting that the steps which are altered are those post uncoating and genome entry. Reduction of infection by cyclodextrin is reversed by increasing MOI whereas that produced by simvastatin treatment is not, suggesting that the effects on infection are not due to a reduction in cholesterol. The differences in the characteristics of inhibition can be explained by the differential effects of the compounds. Cyclodextrin inhibits the store-operated calcium channels, suggesting that reduction in infection is through translational inhibition. Simvastatin produces vesicles from internal membranes which cannot sustain viral RNA synthesis, reducing infection through reduced transcription. The results indicate that the impact on viral infection by the cholesterol-modifying agents is due to the cellular changes produced rather than due to disruption of the cholesterol-rich domains.
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http://dx.doi.org/10.1016/j.bbrc.2006.06.107 | DOI Listing |
Cell Signal
July 2024
Laboratory of Biochemistry and Molecular Biology, Kyoto Pharmaceutical University, Kyoto 607-8414, Japan. Electronic address:
Simvastatin is an inhibitor of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase, which is a rate-limiting enzyme of the cholesterol synthesis pathway. It has been used clinically as a lipid-lowering agent to reduce low-density lipoprotein (LDL) cholesterol levels. In addition, antitumor activity has been demonstrated.
View Article and Find Full Text PDFCell Death Dis
July 2023
Department of Biomedical Sciences, Neuroscience Research Institute, Convergence Research Center for Dementia, Seoul National University College of Medicine, Seoul, 03080, Republic of Korea.
Cell-to-cell propagation of protein aggregates has been implicated in the progression of neurodegenerative diseases. However, the underlying mechanism and modulators of this process are not fully understood. Here, we screened a small-molecule library in a search for agents that suppress the propagation of α-synuclein and mutant huntingtin (mHtt).
View Article and Find Full Text PDFJ Dairy Sci
August 2023
College of Veterinary Medicine, China Agricultural University, Haidian District, Beijing 100193, China; Heilongjiang Provincial Key Laboratory of Prevention and Control of Bovine Diseases, College of Animal Science and Veterinary Medicine, Heilongjiang Bayi Agricultural University, Daqing 163319, China. Electronic address:
Cholesterol in the circulation is partly driven by changes in feed intake, but aspects of cholesterol metabolism during development of fatty liver are not well known. The objective of this study was to investigate mechanisms of cholesterol metabolism in calf hepatocytes challenged with high concentrations of fatty acids (FA). To address mechanistic insights regarding cholesterol metabolism, liver samples were collected from healthy control dairy cows (n = 6; 7-13 d in milk) and cows with fatty liver (n = 6; 7-11 d in milk).
View Article and Find Full Text PDFAm J Physiol Cell Physiol
August 2023
Department of Biological Sciences, College of Arts and Sciences, Ohio University, Athens, Ohio, United States.
Lipid microdomains, ordered membrane phases containing cholesterol and glycosphingolipids, play an essential role in cancer cell adhesion and ultimately metastasis. Notably, elevated levels of cholesterol-rich lipid microdomains are found in cancer cells relative to their normal counterparts. Therefore, alterations of lipid microdomains through cholesterol modulation could be used as a strategy to prevent cancer metastasis.
View Article and Find Full Text PDFToxins (Basel)
May 2022
Institute of Biochemistry, Life Science Center, Vilnius University, LT-10257 Vilnius, Lithuania.
Melittin, the main toxic component in the venom of the European honeybee, interacts with natural and artificial membranes due to its amphiphilic properties. Rather than interacting with a specific receptor, melittin interacts with the lipid components, disrupting the lipid bilayer and inducing ion leakage and osmotic shock. This mechanism of action is shared with pneumolysin and other members of the cholesterol-dependent cytolysin family.
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