Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/38250
標題: Promoter region methylation and reduced expression of thrombospondin-1 after oxygen-glucose deprivation in murine cerebral endothelial cells
作者: 陳全木
Hu, C.J.
Chen, S.D.
Yang, D.I.
Lin, T.N.
Chen, C.M.
Huang, T.H.M.
Hsu, C.Y.
關鍵字: angiogenesis;ischemia;methylation;stroke;thrombospondin-1;altered gene-expression;dna methylation;neuronal injury;messenger-rna;growth-factor;cpg islands;angiogenesis;ischemia;brain;cancer
Project: Journal of Cerebral Blood Flow and Metabolism
期刊/報告no:: Journal of Cerebral Blood Flow and Metabolism, Volume 26, Issue 12, Page(s) 1519-1526.
摘要: 
Angiogenesis is induced in response to ischemia. Thrombospondin-1 (TSP-1) is a potent angiostatic factor. Silencing of TSP-1 expression may contribute to the postischemic angiogenesis. Upregulation of TSP-1, in contrast, may terminate the postischemic angiogenesis. A possible mechanism that silences TSP-1 expression is the DNA methylation of its promoter region. DNA methylation has been reported following cerebral ischemia. The present study aimed to explore whether methylation of the promoter region of TSP-1 regulates its expression after oxygen-glucose deprivation (OGD) in murine cerebral endothelial cells (CECs) in vitro. Sublethal OGD increased the extent of methylation of the promoter region of TSP-1 with a concurrent decrease in TSP-1 mRNA and protein expression in CECs. After reoxygenation, demethylation of the TSP-1 promoter region led to the restoration of TSP-1 mRNA and protein expression. The extent of methylation of the promoter region of TSP-1 was inversely correlated with the extent of TSP-1 gene expression at mRNA and protein levels after OGD. Oxygen-glucose deprivation-induced reduction in the TSP-1 mRNA level was not accompanied by a change in mRNA stability. These findings raise the possibility that OGD downregulation of TSP-1 expression is at least in part due to methylation of its promoter region.
URI: http://hdl.handle.net/11455/38250
ISSN: 0271-678X
DOI: 10.1038/sj.jcbfm.9600304
Appears in Collections:生命科學系所

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