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Microvascular remodeling in ischemic...

Chappell, John C.

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Microvascular remodeling in ischemic mouse skeletal muscle exposed to ultrasonic microbubble destruction: An investigation of mechanisms and therapeutic delivery.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Microvascular remodeling in ischemic mouse skeletal muscle exposed to ultrasonic microbubble destruction: An investigation of mechanisms and therapeutic delivery./
作者:	Chappell, John C.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2007,
面頁冊數:	165 p.
附註:	Source: Dissertations Abstracts International, Volume: 69-07, Section: B.
Contained By:	Dissertations Abstracts International69-07B.
標題:	Biomedical research. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3282479
ISBN:	9780549247609

Microvascular remodeling in ischemic mouse skeletal muscle exposed to ultrasonic microbubble destruction: An investigation of mechanisms and therapeutic delivery.
Chappell, John C.

Microvascular remodeling in ischemic mouse skeletal muscle exposed to ultrasonic microbubble destruction: An investigation of mechanisms and therapeutic delivery. - Ann Arbor : ProQuest Dissertations & Theses, 2007 - 165 p.

Source: Dissertations Abstracts International, Volume: 69-07, Section: B.

Thesis (Ph.D.)--University of Virginia, 2007.

This item must not be sold to any third party vendors.

Recent studies have shown that interactions between low-frequency ultrasound (US) and intravascular microbubbles (MBs) can induce microvascular disruptions that can facilitate the deposition of circulating nanoparticles (NPs) into tissues, as well as potentially enhance vascular remodeling (VR) in normal skeletal muscle and in muscles affected by an arterial occlusion (AO). In the current study, two primary goals were accomplished. Within the first objective, we investigated the notion that US+MB interactions could enhance the VR response in a mouse hindlimb model of ischemia. Based on these results, mechanisms of US+MB-induced neovascularization were examined in the same hindlimb ischemia model using chimeric mice with normal WT and genetically-altered bone marrow-derived cells (BMDCs). Regarding the second broad aim, the spatial distribution of NPs following their US+MB-mediated delivery was detailed, and these observations provided the background for exploring the potential of delivering growth factor-loaded NPs with US+MB interactions in a model of hindlimb ischemia. Within the first general objective, the gracilis muscles (GMs) in ischemic WT mouse hindlimbs exposed to 1-MHz pulsed US and circulating MBs (AO+US+MB group) exhibited significant increases in angiogenesis and arteriogenesis as compared to the contralateral ischemic hindlimb GM exposed to the sham treatment (AO+sham group). The results from the BMDC chimera experiments indicate that US+MB-interactions augment the VR response in ischemic mouse skeletal muscle through the recruitment, but not vascular incorporation, of BMDCs, specifically inflammatory cells (i.e. monocytes), via a CD 18-, but potentially not CCR2-, dependent mechanism. In the second objective, US+MB-treated muscles exhibited significant deposition of NPs into vessel walls and the interstitium. US alone transferred NPs primarily into vessel walls, while MBs alone had no effect on NP delivery. Loaded with either bFGF or BSA, PLGA NPs were administered alongside MBs via a saphenous artery catheter while GMs were exposed to US. As compared to BSA-treated muscles, those exposed to bFGF experienced a significant increase in arteriogenesis, including the diameter enhancement of a GM main feeder vessel (49% increase). Overall, these results demonstrate that US+MB-delivered PLGA NPs loaded with bFGF significantly enhance VR in ischemic mouse hindlimbs, an exciting observation in the development of this potential therapeutic targeted delivery strategy.

ISBN: 9780549247609Subjects--Topical Terms:

3433833
Biomedical research.
Subjects--Index Terms:

Arteriogenesis

Microvascular remodeling in ischemic mouse skeletal muscle exposed to ultrasonic microbubble destruction: An investigation of mechanisms and therapeutic delivery.
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300 $a 165 p.
500 $a Source: Dissertations Abstracts International, Volume: 69-07, Section: B.
500 $a Publisher info.: Dissertation/Thesis.
500 $a Advisor: Price, Richard.
502 $a Thesis (Ph.D.)--University of Virginia, 2007.
506 $a This item must not be sold to any third party vendors.
506 $a This item must not be added to any third party search indexes.
520 $a Recent studies have shown that interactions between low-frequency ultrasound (US) and intravascular microbubbles (MBs) can induce microvascular disruptions that can facilitate the deposition of circulating nanoparticles (NPs) into tissues, as well as potentially enhance vascular remodeling (VR) in normal skeletal muscle and in muscles affected by an arterial occlusion (AO). In the current study, two primary goals were accomplished. Within the first objective, we investigated the notion that US+MB interactions could enhance the VR response in a mouse hindlimb model of ischemia. Based on these results, mechanisms of US+MB-induced neovascularization were examined in the same hindlimb ischemia model using chimeric mice with normal WT and genetically-altered bone marrow-derived cells (BMDCs). Regarding the second broad aim, the spatial distribution of NPs following their US+MB-mediated delivery was detailed, and these observations provided the background for exploring the potential of delivering growth factor-loaded NPs with US+MB interactions in a model of hindlimb ischemia. Within the first general objective, the gracilis muscles (GMs) in ischemic WT mouse hindlimbs exposed to 1-MHz pulsed US and circulating MBs (AO+US+MB group) exhibited significant increases in angiogenesis and arteriogenesis as compared to the contralateral ischemic hindlimb GM exposed to the sham treatment (AO+sham group). The results from the BMDC chimera experiments indicate that US+MB-interactions augment the VR response in ischemic mouse skeletal muscle through the recruitment, but not vascular incorporation, of BMDCs, specifically inflammatory cells (i.e. monocytes), via a CD 18-, but potentially not CCR2-, dependent mechanism. In the second objective, US+MB-treated muscles exhibited significant deposition of NPs into vessel walls and the interstitium. US alone transferred NPs primarily into vessel walls, while MBs alone had no effect on NP delivery. Loaded with either bFGF or BSA, PLGA NPs were administered alongside MBs via a saphenous artery catheter while GMs were exposed to US. As compared to BSA-treated muscles, those exposed to bFGF experienced a significant increase in arteriogenesis, including the diameter enhancement of a GM main feeder vessel (49% increase). Overall, these results demonstrate that US+MB-delivered PLGA NPs loaded with bFGF significantly enhance VR in ischemic mouse hindlimbs, an exciting observation in the development of this potential therapeutic targeted delivery strategy.
590 $a School code: 0246.
650 4 $a Biomedical research. $3 3433833
653 $a Arteriogenesis
653 $a Contrast media
653 $a Controlled release
653 $a Drug delivery
653 $a Ischemic
653 $a Microbubble
653 $a Microvascular remodeling
653 $a Skeletal muscle
653 $a Ultrasound
690 $a 0541
710 2 $a University of Virginia. $3 645578
773 0 $t Dissertations Abstracts International $g 69-07B.
790 $a 0246
791 $a Ph.D.
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793 $a English
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