語系:
繁體中文
English
說明(常見問題)
回圖書館首頁
手機版館藏查詢
登入
回首頁
切換:
標籤
|
MARC模式
|
ISBD
Extracellular matrix regulation in r...
~
Khankan, Rima.
FindBook
Google Book
Amazon
博客來
Extracellular matrix regulation in retinal pigment epithelial cells and role in retinal fibrosis.
紀錄類型:
書目-語言資料,印刷品 : Monograph/item
正題名/作者:
Extracellular matrix regulation in retinal pigment epithelial cells and role in retinal fibrosis./
作者:
Khankan, Rima.
面頁冊數:
138 p.
附註:
Adviser: David R. Hinton.
Contained By:
Dissertation Abstracts International68-03B.
標題:
Health Sciences, Ophthalmology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3257834
Extracellular matrix regulation in retinal pigment epithelial cells and role in retinal fibrosis.
Khankan, Rima.
Extracellular matrix regulation in retinal pigment epithelial cells and role in retinal fibrosis.
- 138 p.
Adviser: David R. Hinton.
Thesis (Ph.D.)--University of Southern California, 2006.
The research in our laboratory is focused on the response of the retinal pigment epithelium (RPE) to injury and how RPE structure and function are altered in pathologic retinal disorders such as proliferative vitreoretinopathy (PVR). RPE cells regulate the balanced homeostasis of growth factors and extracellular matrix (ECM) proteins. We hypothesized that fibronectin EDA (FN-EDA), an ECM molecule implicated in excessive scar formation and chronic fibrosis, is expressed and regulated by activated RPE cells and thus plays an essential role in PVR pathogenesis.Subjects--Topical Terms:
1019445
Health Sciences, Ophthalmology.
Extracellular matrix regulation in retinal pigment epithelial cells and role in retinal fibrosis.
LDR
:03242nam 2200301 a 45
001
945902
005
20110523
008
110523s2006 ||||||||||||||||| ||eng d
035
$a
(UMI)AAI3257834
035
$a
AAI3257834
040
$a
UMI
$c
UMI
100
1
$a
Khankan, Rima.
$3
1269308
245
1 0
$a
Extracellular matrix regulation in retinal pigment epithelial cells and role in retinal fibrosis.
300
$a
138 p.
500
$a
Adviser: David R. Hinton.
500
$a
Source: Dissertation Abstracts International, Volume: 68-03, Section: B, page: 1573.
502
$a
Thesis (Ph.D.)--University of Southern California, 2006.
520
$a
The research in our laboratory is focused on the response of the retinal pigment epithelium (RPE) to injury and how RPE structure and function are altered in pathologic retinal disorders such as proliferative vitreoretinopathy (PVR). RPE cells regulate the balanced homeostasis of growth factors and extracellular matrix (ECM) proteins. We hypothesized that fibronectin EDA (FN-EDA), an ECM molecule implicated in excessive scar formation and chronic fibrosis, is expressed and regulated by activated RPE cells and thus plays an essential role in PVR pathogenesis.
520
$a
Using primary cultures of human RPE cells, we detected FN-EDA protein under normal conditions but not in serum-deprived cells. We found that serum increases the content of FN-EDA in these cultures in a dose-dependent manner. Therefore, all subsequent experiments were carried out in the absence of serum to eliminate any serum-related effects on FN-EDA regulation by RPE cells. In frozen sections of normal human retinas, though FN-EDA was present in retinal and choroidal vessels, the RPE monolayer was devoid of FN-EDA. These results suggest that resting RPE cells do not express FN-EDA.
520
$a
In growth factor-stimulated cultures of RPE cells, we found that FN-EDA mRNA and protein were induced by transforming growth factor-beta2 (TGFbeta2) in a time- and dose-dependent manner but not by connective tissue growth factor (CTGF). By co-stimulating RPE cultures with TGFbeta2 and CTGF, we demonstrated that CTGF, through its N-terminal domain, augments the TGFbeta2-induced expression of FN-EDA at the protein level. Using CTGF domain-specific antibodies, we blocked this synergistic effect. By protein-protein interaction studies, we established that CTGF directly interacts with TGFbeta2 and its receptor TGFbetaRII at its N- and C-terminal domains, respectively. Our results therefore suggest that CTGF modulates TGFbeta2 responses and provide further evidence for CTGF as a down-stream mediator of TGFbeta2.
520
$a
Finally, we demonstrate that FN-EDA is abundantly expressed in PVR membranes in a pattern that co-localizes with TGFbeta2 and CTGF. FN-EDA upregulates type I collagen in cultures of RPE cells as do TGFbeta2 and CTGF. These findings suggest that FN-EDA is an important mediator of retinal fibrosis, making it a potential target for therapy.
590
$a
School code: 0208.
650
4
$a
Health Sciences, Ophthalmology.
$3
1019445
650
4
$a
Health Sciences, Pathology.
$3
1017854
690
$a
0381
690
$a
0571
710
2
$a
University of Southern California.
$3
700129
773
0
$t
Dissertation Abstracts International
$g
68-03B.
790
$a
0208
790
1 0
$a
Hinton, David R.,
$e
advisor
791
$a
Ph.D.
792
$a
2006
856
4 0
$u
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3257834
筆 0 讀者評論
館藏地:
全部
電子資源
出版年:
卷號:
館藏
1 筆 • 頁數 1 •
1
條碼號
典藏地名稱
館藏流通類別
資料類型
索書號
使用類型
借閱狀態
預約狀態
備註欄
附件
W9113706
電子資源
11.線上閱覽_V
電子書
EB W9113706
一般使用(Normal)
在架
0
1 筆 • 頁數 1 •
1
多媒體
評論
新增評論
分享你的心得
Export
取書館
處理中
...
變更密碼
登入