5 Key Takeaways

• 1

  Norepinephrine increased RHOB expression and activity in mouse eyes and human trabecular meshwork cells through β1-adrenergic receptor–cAMP–CREB signaling.

• 2

  RHOB deficiency enhanced trabecular meshwork cell phagocytosis, whereas RHOB overexpression suppressed phagocytosis and reduced cell-layer permeability.

• 3

  The findings support a model in which nocturnal norepinephrine signaling increases RHOB activity, suppresses phagocytosis, and may raise aqueous outflow resistance and nighttime IOP.

• 4

  In mice, RHO and ROCK inhibitors suppressed nocturnal IOP elevation and prevented the IOP increase induced by the β1-adrenergic agonist dobutamine.

• 5

  The study relied heavily on cultured cells and male mice, and the authors noted that circadian norepinephrine release from the superior cervical ganglion has not been clearly established in humans.