Abstract
Recent studies have demonstrated that the expression of miR-34a is significantly upregulated and associated with cell apoptosis in pancreatic β -cell treated with palmitate. Nevertheless, the underlying detailed mechanism is largely unknown. Here, we showed that miR-34a was significantly induced in Min6 pancreatic β -cell upon palmitate treatment. Elevated miR-34a promoted Min6 cell apoptosis. Intriguingly, ectopic expression of miR-34a lowered the expression of Bcl-2, an antiapoptotic protein. Luciferase reporter assay indicated the direct interaction of miR-34a with the Bcl-2 3'-UTR. Moreover, downregulated expression of Bcl-2 induced by palmitate could be restored by inhibition of miR-34a. We conclude that direct suppression of Bcl-2 by miR-34a accounts for palmitate-induced increased apoptosis rate in pancreatic β -cell.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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3' Untranslated Regions
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Animals
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Apoptosis*
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Caspase 3 / chemistry
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Caspase 3 / metabolism
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Cell Line
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Down-Regulation*
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Fatty Acids, Nonesterified / metabolism*
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Gene Expression Regulation
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Gene Silencing
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Genes, Reporter
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Insulin-Secreting Cells / cytology
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Insulin-Secreting Cells / enzymology
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Insulin-Secreting Cells / metabolism*
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Mice
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MicroRNAs / antagonists & inhibitors
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MicroRNAs / metabolism*
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Mutagenesis, Site-Directed
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Mutation
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Palmitic Acid / metabolism*
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Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors*
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Proto-Oncogene Proteins c-bcl-2 / genetics
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Proto-Oncogene Proteins c-bcl-2 / metabolism
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RNA, Small Interfering
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Recombinant Proteins / chemistry
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Recombinant Proteins / metabolism
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Up-Regulation
Substances
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3' Untranslated Regions
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Fatty Acids, Nonesterified
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MIRN34a microRNA, mouse
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MicroRNAs
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Proto-Oncogene Proteins c-bcl-2
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RNA, Small Interfering
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Recombinant Proteins
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Bcl2 protein, mouse
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Palmitic Acid
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Casp3 protein, mouse
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Caspase 3