Dr. Bollag’s expertise is in vitro analysis of signal transduction mechanisms. She has used primary cultures of mouse epidermal keratinocytes for much of her work but recently began applying her expertise to corneal epithelial cells including collaborative studies with Drs. D. Bogorad and P. Gupta, clinicians in the Department of Ophthalmology. Dr. Bollag is an active member of the College of Graduate Studies and has played key leadership roles in the Ph.D. program in Biomedical Science. Her area of vision research is focused on the Phospholipase D2/Aquaporin-3 Signaling Module in cornea. Using the glycerol channel aquaporin-3 (AQP3) knockout mice she has discovered delayed corneal wound healing and proposes that the novel signaling module, PLD2/AQP3/PG, is also involved in regulating corneal epithelial cell function. Her group has succeeded in demonstrating that PLD2 and AQP3 associate in transformed corneal epithelial cells, although the majority of AQP3 is found in heavy, non-caveolin-1-rich membranes. She can alter corneal epithelial cell function by applying phosphatidylglycerol liposomes. Interestingly, different species of PG exert different effects: for example, egg PG (a mixture of several PG species) inhibits corneal epithelial cell migration following wounding whereas dioleoyl-PG enhances their migration to heal wounds. Egg PG also decreased [3H-]thymidine incorporation into DNA, whereas dioleoyl-PG had little or no effect on DNA synthesis. Currently, Dr. Bollag is expanding her studies to normal human corneal epithelial cells.