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Methylation pathway perturbations wi...

Rachlis, Alisa Cheryl.

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Methylation pathway perturbations with folate deficiency: A role for epigenetics in endothelial gene expression.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Methylation pathway perturbations with folate deficiency: A role for epigenetics in endothelial gene expression./
作者:	Rachlis, Alisa Cheryl.
面頁冊數:	168 p.
附註:	Source: Masters Abstracts International, Volume: 42-03, page: 0883.
Contained By:	Masters Abstracts International42-03.
標題:	Biology, Molecular. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=MQ84383
ISBN:	0612843831

Methylation pathway perturbations with folate deficiency: A role for epigenetics in endothelial gene expression.
Rachlis, Alisa Cheryl.

Methylation pathway perturbations with folate deficiency: A role for epigenetics in endothelial gene expression. - 168 p.

Source: Masters Abstracts International, Volume: 42-03, page: 0883.

Thesis (M.Sc.)--University of Toronto (Canada), 2003.

Folate deficiency is an independent risk factor for atherosclerotic cardiovascular disease. To better understand how folate deficiency elicits changes in vascular wall homeostasis, we established an endothelial cell model of folate deficiency. Increases in steady-state mRNA levels of the folate receptor-alpha and gamma-glutamyl hydrolase and an accumulation of cell-associated homocysteine and SAE were found. Because SAH can inhibit many SAM-mediated methylation reactions, we assessed DNA and histone methylation pathways. Genomic cytosine methylation levels indicated global DNA hypomethylation. In agreement with recent evidence indicating that folate bioavailability affects a key endothelial phenotype, namely the production of NO, we found a concentration-dependent decrease in eNOS steady-state mRNA levels. Decreased eNOS promoter RNA polymerase II loading and dimethylated H3-K4 suggested the folate deficiency can alter gene expression by inhibiting methyltransferase pathways. This work describes, for the first time, a novel mechanism by which folate deficiency can confer a predisposition to cardiovascular pathology.

ISBN: 0612843831Subjects--Topical Terms:

1017719
Biology, Molecular.

Methylation pathway perturbations with folate deficiency: A role for epigenetics in endothelial gene expression.
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502 $a Thesis (M.Sc.)--University of Toronto (Canada), 2003.
520 $a Folate deficiency is an independent risk factor for atherosclerotic cardiovascular disease. To better understand how folate deficiency elicits changes in vascular wall homeostasis, we established an endothelial cell model of folate deficiency. Increases in steady-state mRNA levels of the folate receptor-alpha and gamma-glutamyl hydrolase and an accumulation of cell-associated homocysteine and SAE were found. Because SAH can inhibit many SAM-mediated methylation reactions, we assessed DNA and histone methylation pathways. Genomic cytosine methylation levels indicated global DNA hypomethylation. In agreement with recent evidence indicating that folate bioavailability affects a key endothelial phenotype, namely the production of NO, we found a concentration-dependent decrease in eNOS steady-state mRNA levels. Decreased eNOS promoter RNA polymerase II loading and dimethylated H3-K4 suggested the folate deficiency can alter gene expression by inhibiting methyltransferase pathways. This work describes, for the first time, a novel mechanism by which folate deficiency can confer a predisposition to cardiovascular pathology.
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