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Using a gene transfer technique to s...

Smith, Robert Stephen, Jr.

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Using a gene transfer technique to study the role of endothelial nitric oxide synthase in neovascularization and myocardial infarction.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Using a gene transfer technique to study the role of endothelial nitric oxide synthase in neovascularization and myocardial infarction./
作者:	Smith, Robert Stephen, Jr.
面頁冊數:	156 p.
附註:	Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 1702.
Contained By:	Dissertation Abstracts International65-04B.
標題:	Biology, Molecular. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3129378
ISBN:	0496766388

Using a gene transfer technique to study the role of endothelial nitric oxide synthase in neovascularization and myocardial infarction.
Smith, Robert Stephen, Jr.

Using a gene transfer technique to study the role of endothelial nitric oxide synthase in neovascularization and myocardial infarction. - 156 p.

Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 1702.

Thesis (Ph.D.)--Medical University of South Carolina, 2004.

Endothelial nitric oxide synthase (eNOS) plays a vital role in cardiovascular homeostasis. Nitric oxide (NO), generated from eNOS, is involved in various processes including blood pressure regulation, endothelial function, vessel growth, and cardiac function. Cardiovascular ischemic disease results in decreased blood flow and prevents tissues from obtaining vital nutrients, leading to adaptive responses which are in part mediated by NO. In order to elucidate the role of NO in cardiovascular ischemic disease, gene transfer of eNOS using an adenovirus vector was used in models of rat hindlimb ischemia and myocardial infarction.

ISBN: 0496766388Subjects--Topical Terms:

1017719
Biology, Molecular.

Using a gene transfer technique to study the role of endothelial nitric oxide synthase in neovascularization and myocardial infarction.
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245 1 0 $a Using a gene transfer technique to study the role of endothelial nitric oxide synthase in neovascularization and myocardial infarction.
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500 $a Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 1702.
500 $a Director: Julie Chao.
502 $a Thesis (Ph.D.)--Medical University of South Carolina, 2004.
520 $a Endothelial nitric oxide synthase (eNOS) plays a vital role in cardiovascular homeostasis. Nitric oxide (NO), generated from eNOS, is involved in various processes including blood pressure regulation, endothelial function, vessel growth, and cardiac function. Cardiovascular ischemic disease results in decreased blood flow and prevents tissues from obtaining vital nutrients, leading to adaptive responses which are in part mediated by NO. In order to elucidate the role of NO in cardiovascular ischemic disease, gene transfer of eNOS using an adenovirus vector was used in models of rat hindlimb ischemia and myocardial infarction.
520 $a After induction of hindlimb ischemia and eNOS gene delivery, rats showed increased blood perfusion as evidenced by laser Doppler perfusion imaging and a fluorescent microsphere assay compared to rats injected with control virus. Capillary density also significantly increased in eNOS-injected rats. The effects of eNOS gene transfer were abolished by concomitant delivery of adenovirus encoding a dominant negative form of phosphatidylinosiltol-3 kinase (PI3K). In addition, eNOS gene transfer resulted in increased phosphorylation of Akt/PKB in a context of hindlimb ischemia, suggesting that the effects of NO on neovascularization were mediated in part through the PI3K-Akt pathway.
520 $a The effects of eNOS genie delivery were also evaluated in a rat model of myocardial infarction. Six weeks after gene transfer, rats receiving eNOS adenovirus via tail vein injection had improved cardiac performance, attenuation of cardiac hypertrophy and fibrosis, as well as decreased levels of apoptosis compared to rats with MI receiving a control virus. eNOS gene delivery resulted in suppression of oxidative stress induced by MI which led to decreases in TGF-beta1 and p27 expression, JNK activation, and nuclear translocation of NF-kappaB, proteins known to be induced by reactive oxygen species. Taken together, these results suggest that NO protects the heart against left ventricle remodeling by inhibiting oxidative stress induced by MI.
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