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University of Cambridge

Regulation of oligodendrocyte lineage cell function by the RXR$\gamma$ nuclear receptor

Abstract

dc:description.abstract

Remyelination is a spontaneous regenerative process whereby myelin sheaths are restored to demyelinated axons. Key players in this process are oligodendrocyte progenitor cells (OPCs), a widespread population of CNS progenitor cells which persist into adulthood. Remyelination is impaired in patients with chronic demyelinating conditions such as Multiple Sclerosis, and as with other regenerative processes, its efficiency declines with increasing age. Hence, there is a need for the development of therapeutic interventions that will aid in promoting endogenous remyelination when the endogenous regenerative potential is compromised. The nuclear receptor RXRγ is an important positive regulator of OPC differentiation and an accelerator of endogenous remyelination in aged rats. RXRγ functions as a ligand-induced transcription factor and is able to regulate gene transcription. It does so by heterodimerising with other nuclear receptors and recruiting co-regulators involved in chromatin remodelling. However, we lack understanding on the specific mechanism by which RXRγ promotes OPC differentiation. With the work presented in this thesis I demonstrate that RXRγ function is regulated at multiple signalling levels. Proximity ligation assays revealed that RXRγ remains consistently bound to its partners throughout the oligodendrocyte lineage, and the biological relevance of each heterodimer is determined by the dynamic association of co-regulators. This is in turn influenced by ligand presence and subcellular receptor localisation. To identify the genes controlled by RXRγ in OPCs I carried out ChIP sequencing, which revealed genes involved in proliferation and cell cycle control. Further functional assessments aided me in the development of a hypothesis whereby RXRγ activation does not directly influence oligodendrocyte formation, but rather promotes cell cycle exit thereby accelerating and facilitating OPC differentiation. Altered nuclear receptor expression and ligand presence in ageing OPCs may consequently impair this process. My thesis provides an alternative hypothesis to how RXRγ regulates lineage cell progression, highlighting a new avenue in the development of therapeutic interventions targeting generic stem cell functions for which drugs are already FDA approved, rather than oligodendrocyte-specific pathways.

Degree

thesis:*
Name dc:type.qualificationname
Doctor of Philosophy (PhD)
Level dc:type.qualificationlevel
Doctoral
Grantor dc:publisher.institution
University of Cambridge
Year dc:date.issued
2018

Author and committee

dc:creator, dc:contributor.*
Author dc:creator
  • Di Canio, Ludovica
Advisors dc:contributor.advisor
  • Franklin, Robin J. M.
  • Wayne, Gareth

Subjects

dc:subject × 5

Rights

dc:rights
Language dc:language
en

Identifiers

dc:identifier.*
DOI dc:identifier.doi
https://doi.org/10.17863/CAM.36392
OAI identifier oai:identifier
oai:www.repository.cam.ac.uk:1810/289129

Chain of custody

source
Harvested from
Cambridge University
Base URL
api.repository.cam.ac.uk/server/oai/request
Last updated
2026-07-22
Source record
OAI-PMH GetRecord
citation

Di Canio, Ludovica. Regulation of oligodendrocyte lineage cell function by the RXR$\gamma$ nuclear receptor. Doctoral thesis, University of Cambridge, 2018. https://doi.org/10.17863/CAM.36392