{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T04:59:45Z","timestamp":1790312385370,"version":"4.1.0"},"reference-count":75,"publisher":"MDPI AG","issue":"19","license":[{"start":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T00:00:00Z","timestamp":1790121600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"NIH","award":["R01 EY030967"],"award-info":[{"award-number":["R01 EY030967"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Int. J. Mol. Sci.","IJMS"],"abstract":"<jats:p>Topical ocular treatment with glucocorticoids (GCs) yields an increase in intraocular pressure (IOP) in a subset (~35\u201340%) of the human population, known as steroid responders. If treatment is continued, this ocular hypertension (OHT) can develop into GC-induced glaucoma. In mice, the GC-mediated OHT response is modulated by the GC receptor, which exists as two major splice variants, GR\u03b1 and GR\u03b2, in the TM cell cytosol. GR\u03b1 contains a GC-binding domain. Following GC binding, the GR\u03b1-GC complex enters the TM cell nucleus and transactivates genes associated with increased synthesis\/export of extracellular matrix (ECM), causing OHT. GR\u03b2 has no ligand-binding domain but appears to inhibit gene transactivation by the GR\u03b1-GC complex. We previously described the effects of over-expression of GR\u03b2 on the GC-induced OHT response on IOP in mice. Here, we investigated the effect of the GC Dexamethasone (DEX) on the OHT response in C57BL\/6J mice, under conditions of GR\u03b2 knockdown. A total of 20 \u00d7 C57BL\/6J mice (\u2640), aged 3\u20134\u00bd months were used. Animals were weighed. Baseline (BL) conscious IOP measurements (TonoLab) and direct ophthalmoscopy (Keeler Instruments Specialist Model Ophthalmoscope) assessments were made. Animals were divided into 4 cohorts (n = 5\/cohort), and anesthetized (isoflurane (2.5%) and O2(g) (0.8 L\/min)). Cohorts 1 and 2 (n = 10 animals) were given an intravitreal (IVT) injection in both eyes (OU) of Lenti.shRNA.Scramble (2.2 \u00d7 109 TU\/mL; 1 \u03bcL bolus injection (total 2.2 \u00d7 106 TU\/eye)). Cohorts 3 and 4 (n = 10 animals) were given an IVT injection OU of Lenti.shRNA.GR\u03b2 (1.09 \u00d7 109 TU\/mL; 2 \u03bcL bolus injection (total 2.18 \u00d7 106 TU\/eye)). Each subsequent week, for 8 weeks, conscious IOPs were measured (OU), and direct ophthalmoscopy was performed. Animals were then anesthetized and given a periocular injection OU of a 20 \u03bcL bolus (per eye) of either vehicle solution for DEX (DEX-Veh) (Cohorts 1 (n = 5 animals) and 3 (n = 5 animals), or micronized DEX suspension (Cohorts 2 (n = 5 animals) and 4 (n = 5 animals)). At the conclusion of the study, animals were euthanized and TM tissues were collected (OD and OS pooled per animal) for assay of GR\u03b2 mRNA expression using QPCR. GR\u03b2 mRNA expression in the TM was significantly reduced by greater than 95% in the Lenti.shRNA.GR\u03b2 group vs. the Lenti.shRNA.Scramble group (p &lt; 0.0001). Injection of Lenti.shRNA.Scramble or Lenti.shRNA.GR\u03b2 had no effect on baseline IOP. Subsequent injections of DEX over the following 8 weeks led to a significant increase in mean IOP in both groups (baseline 12.5 mmHg; 23 mmHg in Lenti.shRNA.Scramble cohort (p &lt; 0.0001); and 28 mmHg in Lenti.shRNA.GR\u03b2 cohort (p &lt; 0.0001)). DEX-induced IOP was significantly higher in the shRNA.GR\u03b2 cohort compared to the shRNA.Scramble cohort (p &lt; 0.0001). Animals given vehicle control did not show an increase in IOP. Eyes that received DEX had very mild lenticular cataracts at Week 8, but there was no significant reduction in body weight. GR\u03b2 plays a role in modulating the IOP response to DEX in C57BL\/6J mice. Knockdown of endogenous mRNA encoding GR\u03b2 results in an enhanced IOP response to DEX.<\/jats:p>","DOI":"10.3390\/ijms27198483","type":"journal-article","created":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T10:17:26Z","timestamp":1790158646000},"page":"8483","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Knock-Down of Glucocorticoid Receptor Beta (GR\u03b2) Enhances the Ocular Hypertensive Response to Dexamethasone in C57BL\/6J Mice"],"prefix":"10.3390","volume":"27","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6963-500X","authenticated-orcid":false,"given":"J. Cameron","family":"Millar","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Neuroscience, The North Texas Eye Research Institute, University of North Texas Health Fort Worth, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pinkal D.","family":"Patel","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Neuroscience, The North Texas Eye Research Institute, University of North Texas Health Fort Worth, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3594-6560","authenticated-orcid":false,"given":"Abbot F.","family":"Clark","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Neuroscience, The North Texas Eye Research Institute, University of North Texas Health Fort Worth, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2026,9,23]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"324","DOI":"10.1016\/j.ajo.2025.12.013","article-title":"Global Glaucoma Prevalence: Burden and Projection to 2060","volume":"283","author":"Wang","year":"2025","journal-title":"Am. 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