A study found two α2 adrenergic agonists acted directly on meibomian gland (MG) epithelial cells, but the compounds did not elicit a negative effect. While other anti-glaucoma pharmaceuticals timolol and pilocarpine are known to negatively influence such cells, the α2 agonists promoted the their differentiation, researchers found.

In the study, published in Experimental Eye Research, MG epithelial cells were cultured with brimonidine, as well as with clonidine (α2 agonist), phenylephrine (α1 agonist) and two investigational agents—RX821002 (inverse α2 agonist) and MK912 (neutral α2 agonist)—for up to seven days. Cells were counted and evaluated for morphology, signaling pathway activity, protein biomarker expression and the accumulation of neutral lipids, phospholipids and lysosomes.

The findings demonstrated that brimondine treatment induced proliferation and differentiation of MG epithelial cells, including an increase in neutral lipid, phospholipid and lysosome levels, researchers said.¹

Of particular interest, the putative α2 antagonists RX821002 and MK912 did not interfere with brimonidine action, but instead stimulated MG cell differentiation, researchers said.

Overall, the researchers were surprised to find these anti-glaucoma compounds promoted the differentiation of cells rather than eliciting an overall negative effect, as was expected.