BDNF protects retinal neurons from hyperglycemia through the TrkB/ERK/MAPK pathway

Diabetic retinopathy (DR) is one of the most common diabetic eye diseases and a leading cause of blindness. It is characterized by changes in the blood vessels of the retina. The pathogenesis of DR is complex and to date, the precise mechanisms involved remain unclear. Previous studies have reported that DR is associated with neurodegeneration and that apoptosis may occur in diabetic retinas. In the present study, retinal neurons under conditions of hyperglycemia were used as a model to study apoptosis in diabetic retinas. Retinal neurons exposed to hyperglycemia exhibited high levels of apoptosis. Brain-derived neurotrophic factor (BDNF), a member of the neurotrophin family, was effective in protecting retinal neurons from hyperglycemia in vitro. BDNF promoted neuronal cell survival in a concentration-dependent manner. In addition, BDNF was demonstrated to promote the expression of tropomyosin-related kinase B (TrkB) and elevate the phosphorylation levels of TrkB and ERK in retinal neurons exposed to hyperglycemia. The results of the present study demonstrated that BDNF may protect retinal neurons from hyperglycemia via the TrkB/ERK/MAPK pathway and provides novel insights into the pathogenesis of DR.