Advanced glycation end-products induce apoptosis involving the signaling pathways of oxidative stress in bovine retinal pericytes

Chen, Bai-hua; Jiang, Deyong; Tang, Luosheng

doi:10.1016/j.lfs.2006.03.020

Cited by 84 publications

(54 citation statements)

References 38 publications

(52 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A great body of evidence demonstrate that hyperglycemia induces an increased production of ROS, increases the formation of AGEs, which accumulate in microvascular cells in vivo and activates biochemical pathways, such as the hexosamine pathway [36]. On one side, these biochemical changes directly damage retinal cells by disturbed energy metabolism and modification of important intra-and extracellular proteins [37,38]. On the other side, these highly active metabolic intermediates deregulate the expression of important angiogenic and inflammatory cytokines thereby indirectly damage retinal cells [39][40][41].…”

Section: Discussionmentioning

confidence: 99%

Oral Carnosine Supplementation Prevents Vascular Damage in Experimental Diabetic Retinopathy

Pfister

Riedl

Wang

et al. 2011

Cell Physiol Biochem

View full text Add to dashboard Cite

Backgrounds/Aims: Pericyte loss, vasoregression and neuroglial activation are characteristic changes in incipient diabetic retinopathy. In this study, the effect of the antioxidant and antiglycating dipeptide carnosine was studied on the development of experimental diabetic retinopathy. Materials/Methods: STZ-induced diabetic Wistar rats were orally treated with carnosine (1g/kg body weight/day). Retinal vascular damage was assessed by quantitative morphometry. Retinal protein extracts were analyzed for markers of oxidative stress, AGE-formation, activation of the hexosamine pathway and changes in the expression of Ang-2, VEGF and heat shock proteins Hsp27 and HO-1. Glial cell activation was analyzed using Western blot analysis and immunofluorescence of GFAP expression and retinal neuronal damage was histologically examined. Results: Oral carnosine treatment prevented retinal vascular damage after 6 months of experimental hyperglycemia. The protection was not caused by ROS- or AGE-inhibition, but associated with a significant induction of Hsp27 in activated glial cells and normalization of increased Ang-2 levels in diabetic retinas. A significant reduction of photoreceptors in retinas of carnosine treated animals was noted. Conclusion: Oral carnosine treatment protects retinal capillary cells in experimental diabetic retinopathy, independent of its biochemical function. The vasoprotective effect of carnosine might be mediated by the induction of protective Hsp27 in activated glial cells and normalization of hyperglycemia-induced Ang-2.

show abstract

Section: Discussionmentioning

confidence: 99%

Oral Carnosine Supplementation Prevents Vascular Damage in Experimental Diabetic Retinopathy

Pfister

Riedl

Wang

et al. 2011

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…The latter alters the extracellular matrix architecture by nonenzymatic glycation and the formation of protein cross-links. AGEs and RAGE have been proposed as an important pathological mechanism underlying diabetic complications [7], such as diabetic cardiopathy [8], retinopathy [9,10], nephropathy [11][12][13], and atherosclerosis [14,15]. Based on the effect of AGEs and RAGE on other organs, they likely also contribute to GI diabetic complications.…”

Section: Introductionmentioning

confidence: 99%

Up-Regulated Expression of Advanced Glycation End-Products and Their Receptor in the Small Intestine and Colon of Diabetic Rats

Chen

Zhao

2011

Dig Dis Sci

View full text Add to dashboard Cite

show abstract

“…It is also well documented that oxidative stress is linked to AGE formation, and involved in retinal vascular dysfunction. AGEs, in turn, induce oxidative stress via activation of protein kinase C signaling pathways by RAGE, and, thus, to mediate retinal pericyte apoptosis, a histopathologic hallmark of diabetic retinopathy [40].…”

Section: Retinal Endothelial Cells and The Microvasculaturementioning

confidence: 99%

AGEs, RAGE, and Diabetic Retinopathy

2011

View full text Add to dashboard Cite

Diabetic retinopathy is a major diabetic complication with a highly complex etiology. Although there are many pathways involved, it has become established that chronic exposure of the retina to hyperglycemia gives rise to accumulation of advanced glycation end products (AGEs) that play an important role in retinopathy. In addition, the receptor for AGEs (RAGE) is ubiquitously expressed in various retinal cells and is upregulated in the retinas of diabetic patients, resulting in activation of pro-oxidant and proinflammatory signaling pathways. This AGE-RAGE axis appears to play a central role in the sustained inflammation, neurodegeneration, and retinal microvascular dysfunction occurring during diabetic retinopathy. The nature of AGE formation and RAGE signaling bring forward possibilities for therapeutic intervention. The multiple components of the AGE-RAGE axis, including signal transduction, formation of ligands, and the end-point effectors, may be promising targets for strategies to treat diabetic retinopathy.

show abstract

Advanced glycation end-products induce apoptosis involving the signaling pathways of oxidative stress in bovine retinal pericytes

Cited by 84 publications

References 38 publications

Oral Carnosine Supplementation Prevents Vascular Damage in Experimental Diabetic Retinopathy

Oral Carnosine Supplementation Prevents Vascular Damage in Experimental Diabetic Retinopathy

Up-Regulated Expression of Advanced Glycation End-Products and Their Receptor in the Small Intestine and Colon of Diabetic Rats

AGEs, RAGE, and Diabetic Retinopathy

Contact Info

Product

Resources

About