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Endothelin-1 mediated regulation of ...

Rao, Vidhya Ramachandiran.

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Endothelin-1 mediated regulation of extracellular matrix collagens---A role in pathology of primary open angle glaucoma.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Endothelin-1 mediated regulation of extracellular matrix collagens---A role in pathology of primary open angle glaucoma./
Author:	Rao, Vidhya Ramachandiran.
Description:	157 p.
Notes:	Source: Dissertation Abstracts International, Volume: 69-04, Section: B, page: 2256.
Contained By:	Dissertation Abstracts International69-04B.
Subject:	Health Sciences, Ophthalmology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3312850
ISBN:	9780549620181

Endothelin-1 mediated regulation of extracellular matrix collagens---A role in pathology of primary open angle glaucoma.
Rao, Vidhya Ramachandiran.

Endothelin-1 mediated regulation of extracellular matrix collagens---A role in pathology of primary open angle glaucoma. - 157 p.

Source: Dissertation Abstracts International, Volume: 69-04, Section: B, page: 2256.

Thesis (Ph.D.)--University of North Texas Health Science Center at Fort Worth, 2007.

Primary Open Angle Glaucoma (POAG) is a progressive optic neuropathy characterized by loss of retinal ganglion cells, optic nerve degeneration and characteristic extracellular matrix (ECM) remodeling of the optic nerve head. An increase in collagen type I and VI is observed at the level of lamina cribrosa (LC), a distinct connective tissue region of optic nerve head in POAG subjects. Extensive ECM remodeling with enhanced collagen deposition observed in POAG is consistent with the pathology of fibrosis. Mechanisms contributing to ECM remodeling in POAG is not known. Endothelin-1(ET-1), a potent vaso-active peptide plays a key role in glaucoma pathology. Intra-vitreal administration of ET-1 in animal models results in optic neuropathy, RGC apoptosis, axonal transport block and ONA activation. An upregulation of ET-1 and ETB receptors is observed in glaucomatous LC and animal models of glaucoma and ET-1 mediated detrimental effects in POAG appears to be mediated by ET B receptors. ET-1 initiates and maintains enhanced collagen synthesis and deposition in various tissues under pathological conditions and is recognized as a potent profibrotic factor. In the present study we hypothesized that ET-1 increases extracellular matrix collagen deposition in lamina cribrosa and this change in ECM contributes to optic nerve fibrosis.

ISBN: 9780549620181Subjects--Topical Terms:

1019445
Health Sciences, Ophthalmology.

Endothelin-1 mediated regulation of extracellular matrix collagens---A role in pathology of primary open angle glaucoma.
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020 $a 9780549620181
035 $a (UMI)AAI3312850
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040 $a UMI $c UMI
100 1 $a Rao, Vidhya Ramachandiran. $3 1021742
245 1 0 $a Endothelin-1 mediated regulation of extracellular matrix collagens---A role in pathology of primary open angle glaucoma.
300 $a 157 p.
500 $a Source: Dissertation Abstracts International, Volume: 69-04, Section: B, page: 2256.
502 $a Thesis (Ph.D.)--University of North Texas Health Science Center at Fort Worth, 2007.
520 $a Primary Open Angle Glaucoma (POAG) is a progressive optic neuropathy characterized by loss of retinal ganglion cells, optic nerve degeneration and characteristic extracellular matrix (ECM) remodeling of the optic nerve head. An increase in collagen type I and VI is observed at the level of lamina cribrosa (LC), a distinct connective tissue region of optic nerve head in POAG subjects. Extensive ECM remodeling with enhanced collagen deposition observed in POAG is consistent with the pathology of fibrosis. Mechanisms contributing to ECM remodeling in POAG is not known. Endothelin-1(ET-1), a potent vaso-active peptide plays a key role in glaucoma pathology. Intra-vitreal administration of ET-1 in animal models results in optic neuropathy, RGC apoptosis, axonal transport block and ONA activation. An upregulation of ET-1 and ETB receptors is observed in glaucomatous LC and animal models of glaucoma and ET-1 mediated detrimental effects in POAG appears to be mediated by ET B receptors. ET-1 initiates and maintains enhanced collagen synthesis and deposition in various tissues under pathological conditions and is recognized as a potent profibrotic factor. In the present study we hypothesized that ET-1 increases extracellular matrix collagen deposition in lamina cribrosa and this change in ECM contributes to optic nerve fibrosis.
520 $a We have demonstrated that cells of lamina cribrosa (LC) cells, express functional ETA and ETB receptors. ET-1 increases intracellular calcium mobilization via ETA receptors and increases NO release by mechanisms involving both ETA and ETB receptors. Consistent with POAG pathology we have observed an upregulation ETB receptors in LC cells in response to chronic treatment with ET-1. LC cells also express prepro-ET-1, the primary gene transcript of ET-1. We have demonstrated for the first time that ET-1 exerts its profibrotic effects by enhancing collagen type I and type VI mRNA, protein synthesis, deposition and secretion in LC cells. ET-1 enhanced collagen deposition in LC cells appears to involve both ETA and ETB receptors, as both of the receptor antagonist, individually inhibit ET-1 mediated collagen synthesis. We have demonstrated that ET-1 also exerts its profibrotic effects in vivo by enhancing collagen deposition in rat optic nerve head. We have also observed an apparent decrease in ET-1 mediated collagen VI deposition in optic nerve heads of ETB deficient transgenic rats suggesting that ET-1 mediated collagen VI synthesis involves ETB receptor activation.
520 $a In conclusion, endothlein-1 stimulates collagen synthesis and deposition both in vitro in LC cells as well as in vivo at the level of rat optic nerve head. ET-1 mediated increase in collagen synthesis at the level of optic nerve head could render a fibrotic mechanism that contributes to the progression of POAG.
590 $a School code: 1250.
650 4 $a Health Sciences, Ophthalmology. $3 1019445
650 4 $a Health Sciences, Pathology. $3 1017854
650 4 $a Health Sciences, Pharmacology. $3 1017717
690 $a 0381
690 $a 0419
690 $a 0571
710 2 $a University of North Texas Health Science Center at Fort Worth. $3 1021741
773 0 $t Dissertation Abstracts International $g 69-04B.
790 $a 1250
791 $a Ph.D.
792 $a 2007
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3312850