Experimental Ophthalmology - Ocular Cell Biology Laboratory
G. Schlunck
Scar formation after trauma or surgery can hamper vision in a variety of ways, for example by corneal clouding, tractional retinal detachment or sealing of drainage after filtering glaucoma surgery. On the cellular level scarring is induced by cells that evolve into highly contractile myofibroblasts which deposit extracellular matrix material and cause the tissue to shrink as they contract. This process is controlled by growth factors and mechanical forces in a specific interdependent fashion. We study the cellular signaling mechanisms in this process to characterize targets for specific pharmacological intervention.
Meyer-ter-Vehn T, Gebhardt S, Sebald W, Buttmann M, Grehn F, Schlunck G, Knaus P (2006). p38 inhibitors prevent TGF-beta-induced myofibroblast transdifferentiation in human tenon fibroblasts. Invest Ophthalmol Vis Sci 47:1500-9.
Meyer-ter-Vehn T, Sieprath S, Katzenberger B, Gebhardt S, Grehn F, Schlunck G (2006). Contractility as a prerequisite for TGF-beta-induced myofibroblast transdifferentiation in human tenon fibroblasts. Invest Ophthalmol Vis Sci 47: 4895-904.
Meyer-ter-Vehn T, Grehn F, Schlunck G (2008). Localization of TGF-beta type II receptor and ED-A fibronectin in normal conjunctiva and failed filtering blebs. Mol Vis 14: 136-41.
Meyer-ter-Vehn T, Katzenberger B, Han H, Grehn F, Schlunck G (2008). Lovastatin inhibits TGF-beta-induced myofibroblast transdifferentiation in human tenon fibroblasts. Invest Ophthalmol Vis Sci 49: 3955-60.
Intraocular pressure control
Fluid enters the eye through active transport by the ciliary body epithelium at a fairly constant rate. The intraocular pressure is adjusted mainly by modulation of the amount of fluid that leaves the eye through the trabecular meshwork. It is currently unclear, how the intraocular pressure is sensed to drive this regulatory mechanism. Recent evidence supports the idea that the trabecular meshwork itself serves as a mechanosensor to drive a regulatory response in the tissue close to Schlemm's canal. We study cellular signaling mechanisms involved in trabecular meshwork mechanotransduction to identify target molecules for pharmacological reduction of intraocular pressure in glaucoma.
Schlunck G, Han H, Wecker T, Kampik D, Meyer-ter-Vehn T, Grehn F (2008). Substrate rigidity modulates cell-matrix interactions and protein expression in human trabecular meshwork cells. Invest Ophthalmol Vis Sci 49: 262-9.
Our work is supported by the Interdisziplinäres Zentrum für Klinische Forschung (IZKF) Würzburg and Deutsche Forschungsgemeinschaft.