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ABSTRACT: Purpose
Glucocorticoid (GC)-induced ocular hypertension (GC-OHT) is a serious side effect of prolonged GC therapy that can lead to glaucoma and permanent vision loss. GCs cause a plethora of changes in the trabecular meshwork (TM), an ocular tissue that regulates intraocular pressure (IOP). GCs act through the glucocorticoid receptor (GR), and the GR regulates transcription both through transactivation and transrepression. Many of the anti-inflammatory properties of GCs are mediated by GR transrepression, while GR transactivation largely accounts for GC metabolic effects and side effects of GC therapy. There is no evidence showing which of the two mechanisms plays a role in GC-OHT.Methods
GRdim transgenic mice (which have active transrepression and impaired transactivation)
SUBMITTER: Patel GC
PROVIDER: S-EPMC6890434 | biostudies-literature | 2019 May
REPOSITORIES: biostudies-literature