Underlying molecular mechanisms of DIO2 susceptibility in symptomatic osteoarthritis.

ABSTRACT:

Objectives

To investigate how the genetic susceptibility gene DIO2 confers risk to osteoarthritis (OA) onset in humans and to explore whether counteracting the deleterious effect could contribute to novel therapeutic approaches.

Methods

Epigenetically regulated expression of DIO2 was explored by assessing methylation of positional CpG-dinucleotides and the respective DIO2 expression in OA-affected and macroscopically preserved articular cartilage from end-stage OA patients. In a human in vitro chondrogenesis model, we measured the effects when thyroid signalling during culturing was either enhanced (excess T3 or lentiviral induced DIO2 overexpression) or decreased (iopanoic acid).

Results

OA-related changes in methylation at a specific CpG dinucleotide upstream of DIO

SUBMITTER: Bomer N 

PROVIDER: S-EPMC4516000 | biostudies-literature | 2015 Aug

REPOSITORIES: biostudies-literature