- Senior Scientific Officer, NIHR Biomedical Research Centre Musculoskeletal theme
- Director of DPhil and MSc(Res) Taught Courses
Sarah Snelling leads the Soft Tissue Repair Group in NDORMS. She leads the CZI Tendon Seed Network and is a lecturer in Biomedicine at St Hilda's College, Oxford.
Sarah received an MBiochem from the department of Biochemistry, University of Oxford before moving to the Botnar Research Centre, NDORMS to pursue a DPhil in the genetics and functionality of osteoarthritis.
In 2009 Sarah was awarded an Arthritis Research UK Foundation Fellowship at the University of East Anglia. Sarah returned to NDORMS in 2012 as an Arthritis Research UK Career Progression Fellow. During her fellowship Sarah interrogated the in vitro and in vivo role of the Wnt antagonist Dickkopf-3 (Dkk3) in osteoarthritis pathogenesis. In collaborative work with Professor Andrew Carr Sarah has identified inflammatory and fibrotic pathways dysregulated in osteoarthritis and tendinopathy, and characterised cell response to biomaterial scaffolds for cartilage and tendon repair.
Sarah is Senior Scientific Officer for the Musculoskeletal theme of the NIHR Biomedical Research Centre and is Director of taught courses for DPhil and MSc(Res) students at NDORMS.
Osteoarthritis and tendinopathy are characterised by inflammation and fibrosis. Sarah continues to interrogate and characterise the cellular and molecular signatures to enhance identification and testing of repair strategies.
When musculoskeletal soft tissues including tendon become critically damaged by disease or injury surgery is often the only option. Despite improvements in surgical techniques it is common for repairs to fail either structurally or biologically. Implantable scaffolds provide a promising strategy to mechanically strengthen surgical repairs whilst providing cues that guide cell behaviour. Sarah's work characterises the response of endogenous cells to implantable scaffolds. The overarching aim of this research is to use these scaffolds to modify inflammation, potentiate resolution and drive successful, non-fibrotic repair of soft tissues including tendon.
Jayadev C. et al, (2020), Bone & Joint Research, 9, 623 - 632
Rashid MS. et al, (2020), Acta Orthop, 1 - 7
Gacaferi H. et al, (2020), Translational Sports Medicine
INTERLEUKIN-17A, -F, AND -AF INDUCE EXPRESSION OF PRO-INFLAMMATORY GENES IN END-STAGE OSTEOARTHRITIS CHONDROCYTES AND SYNOVIAL FIBROBLASTS
Mimpen JY. et al, (2020), OSTEOARTHRITIS AND CARTILAGE, 28, S113 - S113
Rashid M. et al, (2020), Sci Rep, 10