Related Experiment Videos
Modulation of myocilin/TIGR expression in human trabecular meshwork.
E R Tamm1, P Russell, D L Epstein
1Laboratory of Molecular and Developmental Biology, National Eye Institute, National Institutes of Health, Bethesda, Maryland, USA. ertamm@anatomie.uni-erlangen.de
Investigative Ophthalmology & Visual Science
|October 6, 1999
Summary
Mechanical stimuli maintain myocilin/trabecular meshwork inducible glucocorticoid response protein (TIGR) mRNA expression in human trabecular meshwork (TM). Lack of these stimuli in cell cultures may downregulate TIGR expression.
Area of Science:
- Ophthalmology
- Molecular Biology
- Cell Biology
Background:
- Myocilin, also known as trabecular meshwork inducible glucocorticoid response protein (TIGR), is a key protein in the trabecular meshwork (TM).
- Understanding the regulation of myocilin/TIGR mRNA expression is crucial for comprehending TM function and potential therapeutic targets for glaucoma.
Purpose of the Study:
- To investigate the factors influencing myocilin/TIGR mRNA expression in human TM.
- To compare myocilin/TIGR expression in native TM tissue versus cell cultures.
Main Methods:
- mRNA was isolated from fresh human TM, organ-cultured TM, and primary TM cell lines.
- Full-length myocilin/TIGR cDNA was cloned and used for Northern blot analysis.
- TM cell cultures were treated with dexamethasone, TGF-beta1, and mechanical stretch.
Main Results:
- Myocilin/TIGR mRNA was readily detected in fresh and organ-cultured TM but significantly lower or absent in most TM cell lines.
- Dexamethasone and TGF-beta1 treatment increased myocilin/TIGR mRNA expression in TM cell cultures over time.
- Mechanical stretch also increased myocilin/TIGR mRNA expression, with a faster onset than TGF-beta1.
Conclusions:
- Dynamic mechanical stimuli are essential for maintaining myocilin/TIGR expression in TM in situ.
- The lack of mechanical stimuli in standard monolayer cell cultures may lead to the downregulation of myocilin/TIGR expression, impacting their utility as models.