TY - JOUR
T1 - Effects of glucocorticoids on the trabecular meshwork
T2 - Towards a better understanding of glaucoma
AU - Wordinger, Robert J.
AU - Clark, Abbot F.
N1 - Funding Information:
The authors would like to acknowledge and thank the following organizations for their financial support of our research efforts: The National Glaucoma Program, a program of the American Health Assistance Foundation, Rockville, MD. (Grants NGR-96413 and NGR-98412), The Glaucoma Research Foundation, San Francisco, CA., and Alcon Laboratories, Fort Worth, TX. We also wish to acknowledge and thank Mr. Alfredo Portales Jr. for his medial illustrations which have greatly enhanced this manuscript. In addition we thank Dr. Mitchell D. McCartney for kindly providing Fig. 1 .
PY - 1999/4
Y1 - 1999/4
N2 - Glucocorticoid effects on the human trabecular meshwork can be used as a model system in which to study glaucomatous damage to the trabecular meshwork. One of the most important risk factors for glaucoma is an elevated intraocular pressure. The administration of glucocorticoids also can cause elevated intraocular pressure in some individuals. In addition, there is suggestive evidence linking glucocorticoids with the development of glaucoma. Glucocorticoids cause multiple effects on the human trabecular meshwork including changes in extracellular matrix metabolism, organisation of the cytoskeleton, and changes in gene expression and cell function. New discoveries on the molecular mechanisms of glucocorticoid receptor action provide new opportunities to study the possible role of this receptor in the development of glaucoma. For example, alternate spliced forms of the glucocorticoid receptor, glucocorticoid receptor response element half-sites, numerous modulatory factors, acid direct effects of nuclear transcription factors have been recently described. Other recent information has shown that the new glaucoma gene (GLCIA/myocilin) is induced in the human trabecular meshwork by glucocorticoids. Although the exact function of myocilin is currently unknown, it offers the opportunity to dissect the molecular pathways regulating aqueous humor outflow. Future challenges include determining (1) which glucocorticoid effects in the human trabecular meshwork are responsible for elevated intraocular pressure; and (2) the significance of these findings to the development of glaucoma.
AB - Glucocorticoid effects on the human trabecular meshwork can be used as a model system in which to study glaucomatous damage to the trabecular meshwork. One of the most important risk factors for glaucoma is an elevated intraocular pressure. The administration of glucocorticoids also can cause elevated intraocular pressure in some individuals. In addition, there is suggestive evidence linking glucocorticoids with the development of glaucoma. Glucocorticoids cause multiple effects on the human trabecular meshwork including changes in extracellular matrix metabolism, organisation of the cytoskeleton, and changes in gene expression and cell function. New discoveries on the molecular mechanisms of glucocorticoid receptor action provide new opportunities to study the possible role of this receptor in the development of glaucoma. For example, alternate spliced forms of the glucocorticoid receptor, glucocorticoid receptor response element half-sites, numerous modulatory factors, acid direct effects of nuclear transcription factors have been recently described. Other recent information has shown that the new glaucoma gene (GLCIA/myocilin) is induced in the human trabecular meshwork by glucocorticoids. Although the exact function of myocilin is currently unknown, it offers the opportunity to dissect the molecular pathways regulating aqueous humor outflow. Future challenges include determining (1) which glucocorticoid effects in the human trabecular meshwork are responsible for elevated intraocular pressure; and (2) the significance of these findings to the development of glaucoma.
UR - http://www.scopus.com/inward/record.url?scp=0033036990&partnerID=8YFLogxK
U2 - 10.1016/S1350-9462(98)00035-4
DO - 10.1016/S1350-9462(98)00035-4
M3 - Review article
C2 - 10438153
AN - SCOPUS:0033036990
VL - 18
SP - 629
EP - 667
JO - Progress in Retinal and Eye Research
JF - Progress in Retinal and Eye Research
SN - 1350-9462
IS - 5
ER -