Histone Modifications In Oligodendrocyte Development And Injury

Hypoxia (HX) in very low birth weight preterm infants is the main cause of diffuse whitematter (WM) injury, which is characterized by failed oligodendrocyte progenitor cell (OPC) maturation, loss of oligodendrocytes (OLs), and dysmyelination. Such injury leads to chronic neurological disorders. During normal development, histone modifications promote OPC maturation by altering the accessibility of certain genes to the transcriptional machinery. The objective of the present work is to explore how OPC and OL histones are modified after diffuse WM injury and during recovery in an enriched environment (EE). An in silico analysis of an OPC-specific transcriptome revealed that numerous histone 3 lysine 9 (H3K9) modifying enzymes were differentially expressed following HX and recovery in EE. Then, using Pdgfra-EGFP/Rpl10a transgenic reporter mice (at various postnatal ages), H3K9 acetylation, dimethylation, and trimethylation were quantified in subcortical WM OPCs and OLs using immunohistochemistry. My findings demonstrate that H3K9 modifications are altered by HX and that EE alters injury-induced histone modifications to achieve cellular recovery.

Author

• Wei, Juntian

Language

• en

Date created

• 2021

Type of Work

• Master's Thesis

License

• All rights reserved

Rights statement

• In Copyright

GW Unit

• Bioinformatics and Molecular Biochemistry

Degree

• M.S.

Advisor

• Gallo, Vittorio

Committee Member(s)

• Villagra, Alejandro

Persistent URL

•  https://scholarspace.library.gwu.edu/etd/k643b203s