東華大學圖書館 |

Language: English

Help

回圖書館首頁

手機版館藏查詢

Back

Switch To: Labeled | MARC Mode | ISBD

Coronary perivascular adipose tissue...

Noblet, Jillian Nicole.

Linked to FindBook

Google Book

Amazon

博客來

Coronary perivascular adipose tissue and vascular smooth muscle function: Influence of obesity.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Coronary perivascular adipose tissue and vascular smooth muscle function: Influence of obesity./
Author:	Noblet, Jillian Nicole.
Description:	211 p.
Notes:	Source: Dissertation Abstracts International, Volume: 77-09(E), Section: B.
Contained By:	Dissertation Abstracts International77-09B(E).
Subject:	Physiology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10107419
ISBN:	9781339708201

Coronary perivascular adipose tissue and vascular smooth muscle function: Influence of obesity.
Noblet, Jillian Nicole.

Coronary perivascular adipose tissue and vascular smooth muscle function: Influence of obesity. - 211 p.

Source: Dissertation Abstracts International, Volume: 77-09(E), Section: B.

Thesis (Ph.D.)--Indiana University - Purdue University Indianapolis, 2016.

Factors released from coronary perivascular adipose tissue (PVAT), which surrounds large coronary arteries, have been implicated in the development of coronary disease. However, the precise contribution of coronary PVAT-derived factors to the initiation and progression of coronary vascular dysfunction remains ill defined. Accordingly, this investigation was designed to delineate the mechanisms by which PVAT-derived factors influence obesity-induced coronary smooth muscle dysfunction. Isometric tension studies of coronary arteries from lean and obese swine demonstrated that both lean and obese coronary PVAT attenuate vasodilation via inhibitory effects on smooth muscle K+ channels. Specifically, lean coronary PVAT attenuated KCa and K V7 channel-mediated dilation, whereas obese coronary PVAT impaired K ATP channel-mediated dilation. Importantly, these effects were independent of alterations in underlying smooth muscle function in obese arteries. The PVAT-derived factor calpastatin impaired adenosine dilation in lean but not obese arteries, suggesting that alterations in specific factors may contribute to the development of smooth muscle dysfunction. Further studies tested the hypothesis that leptin, which is expressed in coronary PVAT and is upregulated in obesity, acts as an upstream mediator of coronary smooth muscle dysfunction. Long-term administration (3 day culture) of obese concentrations of leptin markedly altered the coronary artery proteome, favoring pathways associated with calcium signaling and cellular proliferation. Isometric tension studies demonstrated that short-term (30 min) exposure to leptin potentiated depolarization-induced contraction of coronary arteries and that this effect was augmented following longer-term leptin administration (3 days). Inhibition of Rho kinase reduced leptin-mediated increases in coronary artery contractions. Acute treatment was associated with increased Rho kinase activity, whereas longer-term exposure was associated with increases in Rho kinase protein abundance. Alterations in Rho kinase signaling were also associated with leptin-mediated increases in coronary vascular smooth muscle proliferation. These findings provide novel mechanistic evidence linking coronary PVAT with vascular dysfunction and further support a role for coronary PVAT in the pathogenesis of coronary disease.

ISBN: 9781339708201Subjects--Topical Terms:

518431
Physiology.

Coronary perivascular adipose tissue and vascular smooth muscle function: Influence of obesity.
LDR:03271nmm a2200265 4500 001 2075731
005 20161028151544.5
008 170521s2016 ||||||||||||||||| ||eng d
020 $a 9781339708201
035 $a (MiAaPQ)AAI10107419
035 $a AAI10107419
040 $a MiAaPQ $c MiAaPQ
100 1 $a Noblet, Jillian Nicole. $3 3191137
245 1 0 $a Coronary perivascular adipose tissue and vascular smooth muscle function: Influence of obesity.
300 $a 211 p.
500 $a Source: Dissertation Abstracts International, Volume: 77-09(E), Section: B.
500 $a Adviser: Johnathan D. Tune.
502 $a Thesis (Ph.D.)--Indiana University - Purdue University Indianapolis, 2016.
520 $a Factors released from coronary perivascular adipose tissue (PVAT), which surrounds large coronary arteries, have been implicated in the development of coronary disease. However, the precise contribution of coronary PVAT-derived factors to the initiation and progression of coronary vascular dysfunction remains ill defined. Accordingly, this investigation was designed to delineate the mechanisms by which PVAT-derived factors influence obesity-induced coronary smooth muscle dysfunction. Isometric tension studies of coronary arteries from lean and obese swine demonstrated that both lean and obese coronary PVAT attenuate vasodilation via inhibitory effects on smooth muscle K+ channels. Specifically, lean coronary PVAT attenuated KCa and K V7 channel-mediated dilation, whereas obese coronary PVAT impaired K ATP channel-mediated dilation. Importantly, these effects were independent of alterations in underlying smooth muscle function in obese arteries. The PVAT-derived factor calpastatin impaired adenosine dilation in lean but not obese arteries, suggesting that alterations in specific factors may contribute to the development of smooth muscle dysfunction. Further studies tested the hypothesis that leptin, which is expressed in coronary PVAT and is upregulated in obesity, acts as an upstream mediator of coronary smooth muscle dysfunction. Long-term administration (3 day culture) of obese concentrations of leptin markedly altered the coronary artery proteome, favoring pathways associated with calcium signaling and cellular proliferation. Isometric tension studies demonstrated that short-term (30 min) exposure to leptin potentiated depolarization-induced contraction of coronary arteries and that this effect was augmented following longer-term leptin administration (3 days). Inhibition of Rho kinase reduced leptin-mediated increases in coronary artery contractions. Acute treatment was associated with increased Rho kinase activity, whereas longer-term exposure was associated with increases in Rho kinase protein abundance. Alterations in Rho kinase signaling were also associated with leptin-mediated increases in coronary vascular smooth muscle proliferation. These findings provide novel mechanistic evidence linking coronary PVAT with vascular dysfunction and further support a role for coronary PVAT in the pathogenesis of coronary disease.
590 $a School code: 0104.
650 4 $a Physiology. $3 518431
690 $a 0719
710 2 $a Indiana University - Purdue University Indianapolis. $b Cellular and Integrative Physiology. $3 3191138
773 0 $t Dissertation Abstracts International $g 77-09B(E).
790 $a 0104
791 $a Ph.D.
792 $a 2016
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10107419