EPIGENETIC MODIFICATION OF TEN-ELEVEN TRANSLOCATION PROTEIN MEDIATED DNA METHYLATION/DE-METHYLATION IN BRAIN DERIVED NEUROTROPHIC FACTOR FOR THE PATHOGENESIS OF TYPE 2 DIABETIC RETINOPATHY
Author(s):
Vandana Yadav, Mahavir Yadav, Archana Tiwari
Keywords:
Brain derived neurotrophic factor, Epigenetics, Ten-Eleven Translocation protein, Oxidative stress, Retinopathy
Abstract
Type 2 Diabetic Retinopathy is one of the most common complication of diabetes that affect the blood vessels of the retina, leading to blindness. Type 2 Diabetic Retinopathy is a term used for all the abnormalities of the small blood vessels of the retina caused by diabetes. Interaction between genetic and environmental factors in disease development most likely involves epigenetic modifications. The study so far suggested that epigenetics mechanism also play a key role in the pathogenesis of Type 2 Diabetic Retinopathy. BDNF is a neurotrophic factor, previous studies reported that reduced level of BDNF in the diabetic retina may damage neurons, thereby leading to neurodegeneration. The number of studies on various factors such as Vascular Endothelial Growth Factor (VEGF) has been done to prevent Type 2 Diabetic Retinopathy by different mechanisms. Till date, there are no comparable studies available investigating the significance of TET mutations in DNA methylation/de-methylation in BDNF gene, to our knowledge, this is the first report of BDNF methylation/de-methylation status with respect to T2DR. The main concept of the present review focus on epigenetic modification of Ten-Eleven Translocation protein mediated DNA methylation/de-methylation in Brain Derived Neurotrophic Factor for the Pathogenesis of Type 2 Diabetic Retinopathy. BDNF protects retinal neurons from hyperglycemia through the TrkB/ERK/MAPK pathway was reported in past studies. Aim of this review is to study the effect of TET mediated epigenetic modification such as DNA methylation/de-methylation on BDNF gene in case of Type 2 Diabetic Retinopathy.
Article Details
Unique Paper ID: 145358

Publication Volume & Issue: Volume 4, Issue 9

Page(s): 141 - 153
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Last Date 25 June 2018


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