Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/151094
Title: ANALYSIS OF EPIGENETIC MODIFICATIONS IN NEURAL STEM CELLS OF MOUSE EMBRYOS FROM DIABETIC PREGNANCY
Authors: SESHADRI RAMYA
Keywords: miRNA,Maternal diabetes,NTD,hyperglycemia,Sirt1,Mecp2
Issue Date: 24-Aug-2018
Citation: SESHADRI RAMYA (2018-08-24). ANALYSIS OF EPIGENETIC MODIFICATIONS IN NEURAL STEM CELLS OF MOUSE EMBRYOS FROM DIABETIC PREGNANCY. ScholarBank@NUS Repository.
Abstract: Maternal diabetes is known to cause neural tube defects (NTDs) in embryos and neuropsychological deficits in infants. Several metabolic pathways and genes have been identified to be deregulated in developing brain of embryos by maternal diabetes, although the exact mechanism remains unknown. Recently, miRNAs have been shown to regulate brain development and maturation. Therefore, we hypothesized that maternal diabetes alters the expression of small non-coding RNAs called microRNAs(miRNAs) and subsequently the expression of their target genes in neural stem cells (NSCs) thereby resulting in structural or functional malformations in the developing brain. We selected two miRNAs, miR-30b and miR-26b-5p which are predicted to target Sirtuin1 (Sirt1), a histone deacetylase and Methyl CpG binding protein (Mecp2) respectively from microRNA microarray previously done in our lab. We have elucidated the role of Sirt1 in NSC differentiation and role of Mecp2 in synaptogenesis. Overall, these results suggest that maternal diabetes alters genes involved in brain development and patterning via regulating miRNAs resulting in NTDs or neuropsychological deficits.
URI: http://scholarbank.nus.edu.sg/handle/10635/151094
Appears in Collections:Ph.D Theses (Open)

Show full item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
Sesahdri Ramya_Thesis.pdf3.91 MBAdobe PDF

OPEN

NoneView/Download

Page view(s)

44
checked on Jul 10, 2020

Download(s)

3
checked on Jul 10, 2020

Google ScholarTM

Check


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.