Project: A02

There are around 60 million patients with diabetes in the European Union. Diabetics not only suffer from impaired (corneal) wound healing, they also develop various other eye complications such as diabetic retinopathy, macular and corneal edema as well as glaucoma. The disease also affects the corneal epithelium, corneal nerves and tear film. Diabetics show stronger inflammatory reactions after eye surgery, which leads to a higher rate of rejection after corneal transplantation. In this context, impaired inflammatory cell function, reduced secretion of cytokines/growth factors and a prolonged inflammatory phase can be observed in diabetics.

Lymphangiogenesis plays an important role in homeostasis, metabolism and immunity, and also occurs during wound healing. Wound-healing processes lead to the recruitment of macrophages that produce VEGF-C and VEGF-D, and these two factors, in turn, promote lymphangiogenesis. Diabetics, however, show dysfunctional lymphangiogenesis, which slows down the wound-healing process and the recruitment of macrophages. Nevertheless, the detailed mechanism underlying the impaired lymphangiogenesis in diabetes is still elusive.

The goal of this project is to identify novel endogenous factors of inflammatory lymphangiogenesis that play a role in regulating delayed wound healing in diabetic patients using a mouse model that compares collaborative mouse lines with metabolic disorders and thereby using the eye as a model system.

Key methods: QTL analysis, in vivo experiments, IF, image analysis, scRNASeq, cell culture assays (tube formation, migration, proliferation), transfection, qRT-PCR, flow cytometry