Phospholipid secretions of organ cultured ciliary body

Homeostasis of intraocular pressure (IOP) is important for the maintenance of anterior eye anatomic integrity, minimizing pressure‐associated damage to the optic nerve, and maintaining a pressure gradient for blood flow to the eye. IOP is regulated by equilibrium between aqueous humor (AH) production and its outflow. The ciliary body (CB) is thought to actively secrete AH. However, whether AH composition and in particular, its phospholipids are entirely due to CB secretion remains uncertain. Comparison of phospholipids released by cultured CB, phospholipids present within CB tissue, within AH, and within blood and serum are consistent with release of most phospholipids into the AH by the CB. Treatment of CB in culture with timolol, a non‐specific beta‐adrenergic antagonist, alters the release of phospholipids by CB into the media. However, dorzalamide, a carbonic anhydrase inhibitor that reduces production of AH, does not affect phospholipid release thereby suggesting timolol, which also decreases IOP through decreased AH outflow, affects other physiological homeostatic mechanisms regulating aqueous outflow. These outflow changes also affect the composition of secreted phospholipids. We present evidence that release of lipids by the CB has a prolonged survival effect on cultured primary TM cells and TM tissue. Anterior chamber structures such as trabecular meshwork (TM) and fluid: aqueous humor (AH) helps in maintenance of intraocular pressure homeostasis. Our results demonstrate that AH phospholipids, unlike its other constituents, is not entirely produced by the ciliary body (CB). We further demonstrate that the drugs to treat glaucoma such as timolol, alters the release of phospholipids by the CB. We also present evidence that the released CB lipids play a critical role on health and survival of cultured primary TM cells and TM tissue