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

Abstract

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.

Effects of nitrite exposure on haematological parameters, oxidative stress and apoptosis in juvenile turbot (Scophthalmus maximus)

“…Numerous studies indicated that ERK1/2 and JUK could be activated by many environmental stressors or chemical agents via induction of oxidative stress, but this phenomenon was inhibited by treatment with antioxidants Geng et al, 2014;Wang et al, 2014;Zhang et al, 2012). Also, oxidative stress could increase the protein or mRNA levels of MAPKs (Biswas et al, 2012;Liu et al, 2012;Liu et al, 2013). Our study showed that exposure to nitrite increased the mRNA levels of JUK1, implying that the JUK signaling pathways likely played a role in the damage of the turbot gill or branchial cells after nitrite exposure.…”

Environmental Enrichment Protects the Retina from Early Diabetic Damage in Adult Rats

“…In the adult, BDNF expression that enhances and supports brain plasticity is increased by EE housing [45]–[47]. It was shown that serum and retinal levels of BDNF are significantly reduced at early stages of diabetes in rats [48], and BDNF protects retinal neurons from hyperglycemia in vitro [49], supporting that decreased BDNF levels may damage retinal cells early in the course of diabetes. In agreement, BDNF-immunoreactivity decreased in the retina from SE-housed diabetic animals as compared with non-diabetic animals, whereas EE housing prevented the effect of experimental diabetes on BDNF immunoreactivity.…”

Nmnat 1: a Security Guard of Retinal Ganglion Cells (RGCs) in Response to High Glucose Stress

“…Hyperglycemia could lead to the apoptosis of both retinal neurons and vascular cells [28,29]. RGCs are located in the inner retina, and are easily injured in response to high glucose stress.…”