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Regulation of endothelial nitric oxi...

Davis, Michael Elliot.

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Regulation of endothelial nitric oxide synthase expression by laminar shear stress.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Regulation of endothelial nitric oxide synthase expression by laminar shear stress./
作者:	Davis, Michael Elliot.
面頁冊數:	112 p.
附註:	Source: Dissertation Abstracts International, Volume: 64-02, Section: B, page: 0652.
Contained By:	Dissertation Abstracts International64-02B.
標題:	Health Sciences, Pharmacology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3080312

Regulation of endothelial nitric oxide synthase expression by laminar shear stress.
Davis, Michael Elliot.

Regulation of endothelial nitric oxide synthase expression by laminar shear stress. - 112 p.

Source: Dissertation Abstracts International, Volume: 64-02, Section: B, page: 0652.

Thesis (Ph.D.)--Emory University, 2003.

The endothelial nitric oxide synthase (eNOS) produces nitric oxide from L-arginine. One of the most physiologically important stimuli of eNOS expression is unidirectional shear stress. Areas of the vasculature exposed to high shear seem protected from the development of atherosclerosis, while areas exposed to low shear are prone to atherosclerotic lesions. It is thought that shear regulation of eNOS may contribute to this phenomenon.Subjects--Topical Terms:

1017717
Health Sciences, Pharmacology.

Regulation of endothelial nitric oxide synthase expression by laminar shear stress.
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100 1 $a Davis, Michael Elliot. $3 1948370
245 1 0 $a Regulation of endothelial nitric oxide synthase expression by laminar shear stress.
300 $a 112 p.
500 $a Source: Dissertation Abstracts International, Volume: 64-02, Section: B, page: 0652.
500 $a Adviser: David G. Harrison.
502 $a Thesis (Ph.D.)--Emory University, 2003.
520 $a The endothelial nitric oxide synthase (eNOS) produces nitric oxide from L-arginine. One of the most physiologically important stimuli of eNOS expression is unidirectional shear stress. Areas of the vasculature exposed to high shear seem protected from the development of atherosclerosis, while areas exposed to low shear are prone to atherosclerotic lesions. It is thought that shear regulation of eNOS may contribute to this phenomenon.
520 $a Unidirectional shear stress results in a 4--5-fold increase in eNOS mRNA after 6 hours. We found that increased steady state mRNA is a result of a transient increase in transcription, followed by prolonged message stabilization. We identified two separate pathways controlling transcription and stability. We found that eNOS transcription was controlled by a c-Src-dependent, Ras/Raf/MEK/ERK dependent pathway, whereas mRNA stability was also c-Src-dependent, but Ras/Raf/MEK/ERK independent.
520 $a Unidirectional shear stress causes a transient increase in eNOS transcription. Using chimeric eNOS-CAT promoter constructs, we identified a 25 base pair region in the eNOS promoter that is responsive to shear stress. Furthermore, we found that NFkappaB translocated to the nucleus and bound to this region in response to shear. We confirmed these data using a dominant negative IkappaB construct, which inhibited eNOS promoter activity in response to shear.
520 $a We have shown that c-Src plays a role in shear stress stimulation of eNOS expression in cultured cells. To examine the role of c-Src in vivo, we exercised C57Blk/6 and c-Src heterozygous (c-Src+/-) mice for 3 weeks. Exercise increased eNOS protein >2-fold in the aorta and 1.7-fold in the hearts of C57Blk/6 mice while having no effect on eNOS in c-Src+/- mice. Training also increased aortic ecSOD protein expression, which is regulated by NO•, only in C57Blk/6 mice while having no effect in c-Src+/- mice.
520 $a These studies describe the pathway by which unidirectional shear stress increases eNOS expression, and the physiological role of this pathway during exercise training. There are several diseases in which decreased eNOS expression contributes to endothelial dysfunction. Thus, understanding the mechanisms by which shear stress and exercise increase the expression of this beneficial factor may aid in the creation of novel therapeutics targeting vascular disease.
590 $a School code: 0665.
650 4 $a Health Sciences, Pharmacology. $3 1017717
650 4 $a Biology, Cell. $3 1017686
650 4 $a Biology, Molecular. $3 1017719
690 $a 0419
690 $a 0379
690 $a 0307
710 2 0 $a Emory University. $3 1017429
773 0 $t Dissertation Abstracts International $g 64-02B.
790 1 0 $a Harrison, David G., $e advisor
790 $a 0665
791 $a Ph.D.
792 $a 2003
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3080312