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Apolipoprotein A-I inhibits atherosc...

Moore, Ryan E.

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Apolipoprotein A-I inhibits atherosclerosis in vivo by promoting macrophage reverse cholesterol transport and HDL anti-inflammatory and anti-oxidant functions.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Apolipoprotein A-I inhibits atherosclerosis in vivo by promoting macrophage reverse cholesterol transport and HDL anti-inflammatory and anti-oxidant functions./
Author:	Moore, Ryan E.
Description:	237 p.
Notes:	Adviser: Daniel J. Rader.
Contained By:	Dissertation Abstracts International67-12B.
Subject:	Biology, Molecular. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3246206

Apolipoprotein A-I inhibits atherosclerosis in vivo by promoting macrophage reverse cholesterol transport and HDL anti-inflammatory and anti-oxidant functions.
Moore, Ryan E.

Apolipoprotein A-I inhibits atherosclerosis in vivo by promoting macrophage reverse cholesterol transport and HDL anti-inflammatory and anti-oxidant functions. - 237 p.

Adviser: Daniel J. Rader.

Thesis (Ph.D.)--University of Pennsylvania, 2006.

Although it is well established that HDL is anti-atherogenic, the mechanisms by which it inhibits atherosclerosis in vivo have not been definitively proven. The goals of this thesis are fourfold: First, to test the hypothesis that apolipoprotein A-I (apoA-I), the primary protein component of HDL, is directly anti-atherogenic. Second, to determine the in vivo relevance of mechanisms by which apoA-I is presumed to inhibit the development of atherosclerosis. In vitro studies have suggested that apoA-I may promote reverse cholesterol transport, inhibit oxidation, and inhibit inflammation, however the role of apoA-I in these processes in vivo has not been clearly established. Third, to gain a better understanding of HDL anti-atherogenic function, with a particular emphasis on understanding the relationship between apoA-I and HDL function. Lastly, to identify novel mechanisms by which apoA-I may function to inhibit the development of atherosclerosis. In order to pursue these goals we established atherosclerosis-susceptible mouse models of apoA-I deficiency as well as models of transgenic expression and overexpression of human apoA-I. Using these models we determined how apoA-I genotype effected the development of atherosclerosis. In addition we determined how apoA-I genotype influenced the reverse cholesterol transport pathway and HDL anti-oxidant and anti-inflammatory function. To identify novel mechanisms by which apoA-I and HDL function to inhibit the development of atherosclerosis we used both the animal models as well as in vitro studies. Our results indicate that apoA-I is directly anti-atherogenic in vivo, independent of the level of HDL cholesterol. Furthermore, apoA-I is required for efficient reverse cholesterol transport as well as for HDL anti-oxidant and anti-inflammatory functions in vivo. We offer a new connection between the lipid-transporting and anti-oxidant and anti-inflammatory functions of apoA-I by demonstrating that apoA-I is an efficient acceptor of ABCA1-mediated oxidized phospholipid efflux from macrophage cells. In conclusion, apoA-I is directly anti-atherogenic by promotion of macrophage reverse cholesterol transport and HDL antioxidant and anti-inflammatory functions. Strategies to augment the level or functional capacity of apoA-I may represent effective options in the prevention and treatment of cardiovascular disease.Subjects--Topical Terms:

1017719
Biology, Molecular.

Apolipoprotein A-I inhibits atherosclerosis in vivo by promoting macrophage reverse cholesterol transport and HDL anti-inflammatory and anti-oxidant functions.
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100 1 $a Moore, Ryan E. $3 1294721
245 1 0 $a Apolipoprotein A-I inhibits atherosclerosis in vivo by promoting macrophage reverse cholesterol transport and HDL anti-inflammatory and anti-oxidant functions.
300 $a 237 p.
500 $a Adviser: Daniel J. Rader.
500 $a Source: Dissertation Abstracts International, Volume: 67-12, Section: B, page: 6897.
502 $a Thesis (Ph.D.)--University of Pennsylvania, 2006.
520 $a Although it is well established that HDL is anti-atherogenic, the mechanisms by which it inhibits atherosclerosis in vivo have not been definitively proven. The goals of this thesis are fourfold: First, to test the hypothesis that apolipoprotein A-I (apoA-I), the primary protein component of HDL, is directly anti-atherogenic. Second, to determine the in vivo relevance of mechanisms by which apoA-I is presumed to inhibit the development of atherosclerosis. In vitro studies have suggested that apoA-I may promote reverse cholesterol transport, inhibit oxidation, and inhibit inflammation, however the role of apoA-I in these processes in vivo has not been clearly established. Third, to gain a better understanding of HDL anti-atherogenic function, with a particular emphasis on understanding the relationship between apoA-I and HDL function. Lastly, to identify novel mechanisms by which apoA-I may function to inhibit the development of atherosclerosis. In order to pursue these goals we established atherosclerosis-susceptible mouse models of apoA-I deficiency as well as models of transgenic expression and overexpression of human apoA-I. Using these models we determined how apoA-I genotype effected the development of atherosclerosis. In addition we determined how apoA-I genotype influenced the reverse cholesterol transport pathway and HDL anti-oxidant and anti-inflammatory function. To identify novel mechanisms by which apoA-I and HDL function to inhibit the development of atherosclerosis we used both the animal models as well as in vitro studies. Our results indicate that apoA-I is directly anti-atherogenic in vivo, independent of the level of HDL cholesterol. Furthermore, apoA-I is required for efficient reverse cholesterol transport as well as for HDL anti-oxidant and anti-inflammatory functions in vivo. We offer a new connection between the lipid-transporting and anti-oxidant and anti-inflammatory functions of apoA-I by demonstrating that apoA-I is an efficient acceptor of ABCA1-mediated oxidized phospholipid efflux from macrophage cells. In conclusion, apoA-I is directly anti-atherogenic by promotion of macrophage reverse cholesterol transport and HDL antioxidant and anti-inflammatory functions. Strategies to augment the level or functional capacity of apoA-I may represent effective options in the prevention and treatment of cardiovascular disease.
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