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- W2275790782 abstract "Abstract Advanced glycation endproduct(AGE) delays spontaneous apoptosis of human monocytes and contributes to the development of a local inflammatory response. The mechanism by which AGEs effect monocyte apoptosis, however, is unclear. Here we report that AGE-modified BSA and β2-microglobulin(β2m) can increase miR-214 expression in monocytes, which in turn, enhances cell survival by reducing the expression of phosphatase and tensin homolog(PTEN). Employing miRNA microarray, we obtains a genome-wide miRNA expression profiling of THP-1 cells treated with/without AGEs. Among 470 miRNAs screened, 6 miRNAs including miR-214 are upregulated while 5 miRNAs were down-regulated (fold-change>2) in AGE-treated cells. AGE-induced miRNA differential expression is validated by miRNA qRT-PCR. Significant upregulation of miR-214 is confirmed in normal human monocytes treated with AGEs and monocytes isolated from patients with chronic renal failure. Both AGE-treated monocytes and patient monocytes have a delayed apoptosis. Luciferase reporter assay shows that miR-214 targets PTEN mRNA 3’-untranslated region. Furthermore, PTEN expression is inversely correlated with miR-214 expression in monocytes and the forced expression of miR-214 leads to a delayed apoptosis of THP-1. In contrast, decrease of miR-214 expression via anti-miR-214 largely abolishes AGE-induced cell survival. In summary, our findings define a new regulation role of miR-214 on AGE-induced monocyte survival by impeding PTEN expression." @default.
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- W2275790782 date "2010-04-01" @default.
- W2275790782 modified "2023-09-29" @default.
- W2275790782 title "Role of microRNA-214-targeting PTEN in advanced glycation endproducts-induced apoptosis delay of monocytes (89.35)" @default.
- W2275790782 doi "https://doi.org/10.4049/jimmunol.184.supp.89.35" @default.
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