RNA Isolation in Duchenne Muscular Dystrophy (DMD) Mice Models

Fibrosis is a progressive and typically irreversible disease process characterized by the excessive deposition of collagen in organs and in tissues of the musculoskeletal (MSK) system1,2. This process, which causes loss of organ and tissue function, can be initiated by micro-traumas3, an excessive and/or prolonged immune response1, the activation and proliferation of fibrosis-inducing progenitor cells4, and a pro-fibrotic extra-cellular microenvironment5. In parallel with the events that initiate fibrosis, genetic or environmental influences may cause cells and tissues to become predisposed to fibrosis development prior to initiation. This suggests that these cells and tissues are in a state of prodromal disease6, 7, i.e. a hypersensitive state that is distinct from both active fibrosis and normal homeostasis, where cells and tissues are “primed” for fibrosis development. The ability to detect cells or tissues in this state would be extremely valuable in the clinic, as it would identify patients at risk of fibrosis and facilitate pre-emptive therapeutic interventions before irreversible tissue damage has occurred. Investigation into Duchenne Muscular Dystrophy (DMD) mice models can provide valuable insights into fibrosis. Through analysis and comparison of RNA sequence data from 8-week-old pre-fibrotic mdx mice (dystrophin-/-/utrophin+/+) and wildtype mice (dystrophin+/+/utrophin+/+) potential bio markers for fibrosis can be identified. Future research can be directed towards these bio markers in patients predisposed to or suffering from DMD.