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Studies on the antiangiogenic action...

Lee, Hsinyu.

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Studies on the antiangiogenic action of 16K PRL: Regulation of urokinase-type plasminogen activator system.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Studies on the antiangiogenic action of 16K PRL: Regulation of urokinase-type plasminogen activator system./
作者:	Lee, Hsinyu.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 1998,
面頁冊數:	153 p.
附註:	Source: Dissertations Abstracts International, Volume: 60-07, Section: B.
Contained By:	Dissertations Abstracts International60-07B.
標題:	Cellular biology. -
電子資源:	https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9903304
ISBN:	9780599005075

Studies on the antiangiogenic action of 16K PRL: Regulation of urokinase-type plasminogen activator system.
Lee, Hsinyu.

Studies on the antiangiogenic action of 16K PRL: Regulation of urokinase-type plasminogen activator system. - Ann Arbor : ProQuest Dissertations & Theses, 1998 - 153 p.

Source: Dissertations Abstracts International, Volume: 60-07, Section: B.

Thesis (Ph.D.)--University of California, San Francisco, 1998.

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

Angiogenesis is regulated by both stimulatory and inhibitory substances, namely angiogenic and antiangiogenic factors, respectively. An essential step in the regulation of angiogenesis is the regulation of uPA which in turn activates a cascade of proteases which play essential roles in endothelial cell migration and tissue remodeling. Work described in this thesis focuses on the effect of the antiangiogenic factor 16K PRL on urokinase activity in BBE cells. We show that 16K PRL inhibits bFGF-stimulated uPA activity and migration of BBE cells. 16K PRL has no effect on uPA mRNA levels; however, it stimulates the expression of the protein levels of PAI-1, a major inhibitor for uPA activity. The stimulatory effect of 16K PRL on PAI-1 appears to be at the transcriptional levels since 16K PRL increase PAI-1 mRNA levels while it has no effect on the stability of PAI-1 mRNA. We further investigated the signaling mechanisms mediated by 16K PRL to stimulate PAI-1. By using kinase inhibitor, we show that 16K PRL PAI-1 is mediated through a serine/threonine kinase which is neither PKC nor PKA. Moreover, by luciferase reporter experiments, we show that the response element of 16K PRL is located between $-$6.4 kb and $-$1.5 kb region of the human PAI-1 promoter, which is different from the known TGF $\\beta$ response element located within the first 800 bp of this promoter. These results suggest that 16K PRL and TGF $\\beta$ are mediated through a similar but distinct signaling mechanism. Data presented also show that the members of 16K hPRL family members, including 16K hGH, 16K hGHV and 16K hPL, all stimulate PAI-1 production, while their full length counterparts have no effect. The signaling is not mediated through a intact GH or PRL receptor. Moreover, a serine/threonine kinase-dependent signaling mechanism is utilized by all these fragments to stimulate PAI-1. These findings suggest that the antiangiogenic effect of these factors are mediated through a same or similar family of receptors which is neither GH or PRL receptor.

ISBN: 9780599005075Subjects--Topical Terms:

3172791
Cellular biology.
Subjects--Index Terms:

Angiogenesis

Studies on the antiangiogenic action of 16K PRL: Regulation of urokinase-type plasminogen activator system.
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300 $a 153 p.
500 $a Source: Dissertations Abstracts International, Volume: 60-07, Section: B.
500 $a Publisher info.: Dissertation/Thesis.
500 $a Advisor: Weiner, Richard.
502 $a Thesis (Ph.D.)--University of California, San Francisco, 1998.
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 Angiogenesis is regulated by both stimulatory and inhibitory substances, namely angiogenic and antiangiogenic factors, respectively. An essential step in the regulation of angiogenesis is the regulation of uPA which in turn activates a cascade of proteases which play essential roles in endothelial cell migration and tissue remodeling. Work described in this thesis focuses on the effect of the antiangiogenic factor 16K PRL on urokinase activity in BBE cells. We show that 16K PRL inhibits bFGF-stimulated uPA activity and migration of BBE cells. 16K PRL has no effect on uPA mRNA levels; however, it stimulates the expression of the protein levels of PAI-1, a major inhibitor for uPA activity. The stimulatory effect of 16K PRL on PAI-1 appears to be at the transcriptional levels since 16K PRL increase PAI-1 mRNA levels while it has no effect on the stability of PAI-1 mRNA. We further investigated the signaling mechanisms mediated by 16K PRL to stimulate PAI-1. By using kinase inhibitor, we show that 16K PRL PAI-1 is mediated through a serine/threonine kinase which is neither PKC nor PKA. Moreover, by luciferase reporter experiments, we show that the response element of 16K PRL is located between $-$6.4 kb and $-$1.5 kb region of the human PAI-1 promoter, which is different from the known TGF $\\beta$ response element located within the first 800 bp of this promoter. These results suggest that 16K PRL and TGF $\\beta$ are mediated through a similar but distinct signaling mechanism. Data presented also show that the members of 16K hPRL family members, including 16K hGH, 16K hGHV and 16K hPL, all stimulate PAI-1 production, while their full length counterparts have no effect. The signaling is not mediated through a intact GH or PRL receptor. Moreover, a serine/threonine kinase-dependent signaling mechanism is utilized by all these fragments to stimulate PAI-1. These findings suggest that the antiangiogenic effect of these factors are mediated through a same or similar family of receptors which is neither GH or PRL receptor.
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