.Dr. Feener's laboratory performs basic research on biochemical and cellular mechanisms that mediate the vascular complications of diabetes, especially diabetic retinopathy and stroke. A major focus of his laboratory is on the contributions of the kallikrein kinin system and intrinsic coagulation cascade on vasogenic edema, neuronal dysfunction, hemostasis, and thrombosis.
Diabetic macular edema (DME) is a leading cause of vision loss. Although anti-VEGF therapies are often effective in improving vision and reducing macular thickness in patients with DME, a large proportion of patients do not fully respond to this approach. A major goal of the Feener lab is the identification of VEGF-independent mechanisms that contribute to DME. The laboratory utilizes a combination of research strategies including proteomics of human ocular fluids, mechanistic and imaging studies using animal models, and molecular and biochemical analyses. This work has led to the identification of the plasma kallikrein kinin system as a potential cause of DME. Studies are currently investigating the effects of the plasma kallikrein and its downstream effectors, including kinins and of the intrinsic coagulation cascade components, on retinal edema and visual function in rodent models of diabetic retinopathy.
Cerebrovascular Disease and Stroke
Diabetes increases the risk and worsens the outcomes of stroke, which is a major cause of mortality and adult disability. Dr. Feener's laboratory investigates the effects of diabetes on cerebral hemorrhage and ischemia-induced edema and infarction. Studies are ongoing to characterize the role of plasma kallikrein and the intrinsic coagulation system on vascular permeability, edema, and hematoma expansion during stroke in the presence of high blood glucose. Studies are also underway to characterize the role of the plasma kallikrein system on vascular, glial, and neuron dysfunction and cell death during stroke in diabetic rodent models.