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Role of glucocorticoid receptor beta...

University of North Texas Health Science Center at Fort Worth.

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Role of glucocorticoid receptor beta in glucocorticoid-induced ocular hypertension.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Role of glucocorticoid receptor beta in glucocorticoid-induced ocular hypertension./
Author:	Jiang, Ming.
Description:	75 p.
Notes:	Source: Masters Abstracts International, Volume: 47-04, page: 2169.
Contained By:	Masters Abstracts International47-04.
Subject:	Biology, Molecular. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=1462950
ISBN:	9781109019384

Role of glucocorticoid receptor beta in glucocorticoid-induced ocular hypertension.
Jiang, Ming.

Role of glucocorticoid receptor beta in glucocorticoid-induced ocular hypertension. - 75 p.

Source: Masters Abstracts International, Volume: 47-04, page: 2169.

Thesis (M.S.)--University of North Texas Health Science Center at Fort Worth, 2008.

Keywords. glaucoma; glucocorticoid; glucocorticoid receptor beta; trabecular meshwork

ISBN: 9781109019384Subjects--Topical Terms:

1017719
Biology, Molecular.

Role of glucocorticoid receptor beta in glucocorticoid-induced ocular hypertension.
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005 20100708
008 100708s2008 ||||||||||||||||| ||eng d
020 $a 9781109019384
035 $a (UMI)AAI1462950
035 $a AAI1462950
040 $a UMI $c UMI
100 1 $a Jiang, Ming. $3 1021898
245 1 0 $a Role of glucocorticoid receptor beta in glucocorticoid-induced ocular hypertension.
300 $a 75 p.
500 $a Source: Masters Abstracts International, Volume: 47-04, page: 2169.
502 $a Thesis (M.S.)--University of North Texas Health Science Center at Fort Worth, 2008.
520 $a Keywords. glaucoma; glucocorticoid; glucocorticoid receptor beta; trabecular meshwork
520 $a Purpose. Previous studies from our laboratory have shown that glaucomatous trabecular meshwork (TM) cells have a lower expression of glucocorticoid receptor beta (GRbeta) compared to normal TM cells. Overexpression of glucocorticoid receptor beta was found to attenuate glucocorticoid responsiveness in glaucomatous TM cells. The purpose of this study was to determine if downregulating GRbeta expression could increase glucocorticoid responsiveness in cultured transformed normal trabecular meshwork cells (NTM5 cells) and primary trabecular meshwork cell lines derived from normal individuals. Methods. siRNA oligonucleotide sequences specific for GRbeta were designed, cloned into expression vectors and sequenced. TM cells were transfected with different siRNA constructs for GRbeta, while a scrambled sequence served as a negative control. Immunoblot analyses were carried out in the transfected TM cells to determine knockdown of GRbeta expression. In another set of experiments TM cells were transfected with either a GRbeta siRNA contruct or an empty vector (control) and co-transfected with a GRbeta-luciferase reporter and a SV40 promoter-beta galactosidase construct to normalize for efficiency of transfection. Promoter-reporter assays were carried out to determine the effect of GRbeta knockdown on glucocorticoid-mediated luciferase reporter activity. Results. Using Metafectene(TM) pro as the transfection reagent for siRNA, an appreciable 50% to 90% decrease in GRbeta protein expression was observed 72 hours post-transfection in three GRbeta siRNA constructs transfected in NTM5 cells, compared to the scrambled sequence transfected cells. NTM5 cells transfected with the empty vector (control) showed a 3.5 fold increase in luciferase activity after dexamethasone treatment, which was further increased (4 to 5 fold) by knocking down GRbeta expression using a siRNA construct specific for GRbeta. A similar trend was found using GRbeta-siRNA#3 to transient knockdown GRbeta in four primary TM cell lines---NTM210-05, NTM486-04. NTM174-04, and NTM153-00, respectively. To investigate the glucocorticoid responsiveness in cells permanently transfected for knockdown of GRbeta, we made 6 clones from NTM5 cells. There were 10 to 20 fold induction in luciferase activity in GRbeta siRNA stably transfected NTM5 cells, following glucocorticoid administration, respectively. Conclusion. In this study, using RNAi(s) which is specific for GRbeta, we decreased GRbeta expression in vitro in several different cell lines. Using luciferase assays it was found that the glucocorticoid responsiveness after knockdown of GRbeta in vitro in trabecular meshwork cells was significantly enhanced. Decreased GRbeta expression significantly increased glucocorticoid responsiveness not only in normal transformed human trabecular meshwork cells (NTM5 cells), but also in four primary trabecular meshwork (TM) cell lines derived from normal individuals. These results further support the notion that GRbeta negatively regulates glucocorticoid responsiveness in TM cells.
590 $a School code: 1250.
650 4 $a Biology, Molecular. $3 1017719
650 4 $a Health Sciences, Ophthalmology. $3 1019445
650 4 $a Health Sciences, Pharmacology. $3 1017717
690 $a 0307
690 $a 0381
690 $a 0419
710 2 $a University of North Texas Health Science Center at Fort Worth. $3 1021741
773 0 $t Masters Abstracts International $g 47-04.
790 $a 1250
791 $a M.S.
792 $a 2008
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=1462950