Journal of Clinical and Experimental Ophthalmology
Open Access
ISSN: 2155-9570
+44 1223 790975
ISSN: 2155-9570
+44 1223 790975
Nikhat Ahmed
Accepted Abstracts: J Clin Exp Ophthalmol
This is the first report to show that epigenetic mechanisms are critical regulators of gene expression in ocular disorders. A link between corneal epithelial wound healing and expression of DNMT-1 and DNMT-3b, proposing DNA methylation as one of the underlying regulatory mechanism. The concept of gene de-repression will be critical for furthering our understanding of the complex process of corneal epithelial wound healing. In this study we introduced a new layer of control involving DNMTs that keep these genes silent during unwounded conditions (controls) but active during critical times of wound repair. Identification of such mechanisms could be useful in developing new corneal therapies, especially from the point of drug development. Additionally RNA interference-mediated knock down of DNMT1 in non-migrating controls and DNMT3b in migrating cells results in hypomethylation facilitating cell migration and in the latter case retarded cell migration. The inhibitors of DNA methylation have profound effect on the DNMT1 and 3b. As these genes play a role in extracellular matrix remodelling and cell adhesion, their dysregulation may contribute to development of intact epithelial layer. Our findings suggest that DNA methylation has a key role in regulating expression of genes which are involved in HCEC migration.
Nikhat Ahmed is a Professor of Biochemistry with a Ph.D. in Neurochemistry from the University of Surrey, England (1981) and post-doctoral from the department of Ophthalmology at School of Medicine, Tuft?s University, Boston, MA. She has worked on the Membrane Proteome Initiatives of AOHUPO and has been has been leading projects of Disease Proteomics, covering the fields of proteomics, biochemistry, molecular and cellular biology both nationally and internationally, since then. She has published more than 50 papers in reputed journals.