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Developing a mouse model of Pulmonar...

Goldthorpe, Heather Anne Margaret.

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Developing a mouse model of Pulmonary Arterial Hypertension through over-expression of an endothelial-specific fas-inducing apoptosis construct.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Developing a mouse model of Pulmonary Arterial Hypertension through over-expression of an endothelial-specific fas-inducing apoptosis construct./
Author:	Goldthorpe, Heather Anne Margaret.
Description:	105 p.
Notes:	Source: Masters Abstracts International, Volume: 52-06.
Contained By:	Masters Abstracts International52-06(E).
Subject:	Molecular biology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=MS26736
ISBN:	9780499267368

Developing a mouse model of Pulmonary Arterial Hypertension through over-expression of an endothelial-specific fas-inducing apoptosis construct.
Goldthorpe, Heather Anne Margaret.

Developing a mouse model of Pulmonary Arterial Hypertension through over-expression of an endothelial-specific fas-inducing apoptosis construct. - 105 p.

Source: Masters Abstracts International, Volume: 52-06.

Thesis (M.Sc.)--University of Ottawa (Canada), 2014.

Pulmonary arterial hypertension (PAH) is a lethal disease, characterized by functional or structural abnormalities involving distal pulmonary arterioles that result in increased pulmonary vascular resistance (PVR) and ultimately right heart failure. Our objective is to establish a conditional transgenic system in mice, to test the hypothesis that lung EC apoptosis at the level of distal pulmonary arterioles is necessary and sufficient to cause a PAH phenotype. In a pilot study, the Fas-Induced Apoptosis (FIA) construct was expressed under the control of endothelial-specific Tie2 promoter in transgenic mice (i.e. EFIA mice). Administration of a small molecule dimerizing agent, AP20187, resulted in lung modest dose-dependent PAH, which was associated with proliferative vascular lesions localized to distal lung arterioles in a small proportion of mice. Due to the low level of transgene expression in preliminary EFIA lines, we re-designed the transgenic vector by incorporating a more robust endothelial promoter (superTie2). The new construct was transfected into HUVEC and BAEC and analyzed by monitoring immunofluorescence (DsRed). Data from the EFIA model suggests that EC apoptosis may be sufficient to induce a PAH phenotype with the characteristic lung vascular lesions. The EFIA model will allow us to better explore the mechanism that links distal lung EC apoptosis with reactive vascular cell proliferation in the pathogenesis of this devastating disease.

ISBN: 9780499267368Subjects--Topical Terms:

517296
Molecular biology.

Developing a mouse model of Pulmonary Arterial Hypertension through over-expression of an endothelial-specific fas-inducing apoptosis construct.
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100 1 $a Goldthorpe, Heather Anne Margaret. $3 3185321
245 1 0 $a Developing a mouse model of Pulmonary Arterial Hypertension through over-expression of an endothelial-specific fas-inducing apoptosis construct.
300 $a 105 p.
500 $a Source: Masters Abstracts International, Volume: 52-06.
502 $a Thesis (M.Sc.)--University of Ottawa (Canada), 2014.
520 $a Pulmonary arterial hypertension (PAH) is a lethal disease, characterized by functional or structural abnormalities involving distal pulmonary arterioles that result in increased pulmonary vascular resistance (PVR) and ultimately right heart failure. Our objective is to establish a conditional transgenic system in mice, to test the hypothesis that lung EC apoptosis at the level of distal pulmonary arterioles is necessary and sufficient to cause a PAH phenotype. In a pilot study, the Fas-Induced Apoptosis (FIA) construct was expressed under the control of endothelial-specific Tie2 promoter in transgenic mice (i.e. EFIA mice). Administration of a small molecule dimerizing agent, AP20187, resulted in lung modest dose-dependent PAH, which was associated with proliferative vascular lesions localized to distal lung arterioles in a small proportion of mice. Due to the low level of transgene expression in preliminary EFIA lines, we re-designed the transgenic vector by incorporating a more robust endothelial promoter (superTie2). The new construct was transfected into HUVEC and BAEC and analyzed by monitoring immunofluorescence (DsRed). Data from the EFIA model suggests that EC apoptosis may be sufficient to induce a PAH phenotype with the characteristic lung vascular lesions. The EFIA model will allow us to better explore the mechanism that links distal lung EC apoptosis with reactive vascular cell proliferation in the pathogenesis of this devastating disease.
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