Contact information

Email	sarah.snelling@ndorms.ox.ac.uk
Tel	+44 (0)1865 (2)23423

My connections

Fibrotic signaling in OA Research project
Carr Group | Regenerative Medicine Research Group

Centre for OA Pathogenesis Research Group

Sarah Snelling

MBiochem DPhil

Senior Research Fellow

Senior Scientific Officer, NIHR Biomedical Research Centre Musculoskeletal theme
Director of DPhil and MSc(Res) Taught Courses

Biography

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. During this fellowship. Sarah returned to NDORMS in 2012 as an Arthritis Research UK Career Progression Fellow. During her fellowship studies Sarah identified the Wnt antagonist Dickkopf-3 (Dkk3) as upregulated in osteoarthritis and interrogated its in vitro and in vivo role in osteoarthritis pathogenesis. Dkk3 was shown to regulate the response of cartilage to injury and inflammation and to regulate fibrotic signaling pathways including TGFβ. During this time Sarah pursued collaborative research with Professor Andrew Carr's research group that identified inflammatory and fibrotic pathways dysregulated in osteoarthritis and tendinopathy, and characterised cell response to biomaterial scaffolds for cartilage and tendon regeneration.

In 2016 Sarah was appointed as a Senior Research Fellow at NDORMS and is the academic lead for a programme of research focusing on the interaction of cells with biomaterials. In 2017 she became the senior scientific officer for the musculoskeletal theme of the NIHR Biomedical Research Centre where she manages interactions with other themes and is responsible for scientific reporting of the musculoskeletal theme. Sarah is also the Director of taught courses for DPhil and MSc(Res) students at NDORMS.

Research Summary

There is a critical need for improved biological understanding and clinical outcome in fibrotic diseases of musculoskeletal soft tissues including tendinopathy and osteoarthritis. Fibrotic and inflammatory signalling pathways are disrupted in osteoarthritis and tendinopathy and Sarah continues to interrogate and characterise these pathways in collaboration with Dr Stephanie Dakin and Prof. Andrew Carr.

When musculoskeletal soft tissues including tendon become critically damaged surgery is the only clinical option. However, despite improvements in surgical techniques, the success of current surgical repairs is limited. Biomaterial scaffolds provide a promising strategy to biologically and structurally enhance this repair. We know that the activity of disease-relevant cells can be altered by changing the chemical and physical properties of biomaterials. This has led to Sarah’s current research on the mechanisms underlying cell response to biomaterials.

This work aims to harness the biomaterial response of endogenous cells to modify inflammation, potentiate resolution and ultimately drive successful, non-fibrotic repair of soft tissues including tendon.

Resorbable electrospun polydioxanone fibres modify the behaviour of cells from both healthy and diseased human tendons.
Kendal A. et al, (2017), Eur Cell Mater, 33, 169 - 182
Presence of IL-17 in synovial fluid identifies a potential inflammatory osteoarthritic phenotype.
Snelling SJ. et al, (2017), PLoS One, 12
Differential expression of alarmins-S100A9, IL-33, HMGB1 and HIF-1α in supraspinatus tendinopathy before and after treatment.
Mosca MJ. et al, (2017), BMJ Open Sport Exerc Med, 3
Identifying the optimum source of mesenchymal stem cells for use in knee surgery.
Davies BM. et al, (2016), J Orthop Res
Biocompatibility of implantable materials: An oxidative stress viewpoint.
Mouthuy PA. et al, (2016), Biomaterials, 109, 55 - 68
Profibrotic mediators in tendon disease: a systematic review.
Morita W. et al, (2016), Arthritis Res Ther, 18
A comparative evaluation of the effect of polymer chemistry and fiber orientation on mesenchymal stem cell differentiation.
Rowland DC. et al, (2016), J Biomed Mater Res A, 104, 2843 - 2853
H3K27me3 demethylases regulate in vitro chondrogenesis and chondrocyte activity in osteoarthritis.
Yapp C. et al, (2016), Arthritis Res Ther, 18
Dickkopf-3 is upregulated in osteoarthritis and has a chondroprotective role.
Snelling SJ. et al, (2016), Osteoarthritis Cartilage, 24, 883 - 891
H3K27ME3 DEMETHYLASES REGULATE IN VITRO CHONDROGENESIS AND CHONDROCYTE ACTIVITY IN OSTEOARTHRITIS
Yapp C. et al, (2016), OSTEOARTHRITIS AND CARTILAGE, 24, S181 - S181
Comparison of transforming growth factor beta expression in healthy and diseased human tendon.
Goodier HC. et al, (2016), Arthritis Res Ther, 18
The response of tenocytes to commercial scaffolds used for rotator cuff repair.
Smith RD. et al, (2016), Eur Cell Mater, 31, 107 - 118
The response of tenocytes to commercial scaffolds used for rotator cuff repair.
Smith RD. et al, (2016), Eur Cell Mater, 31, 107 - 118
The chondrocyte-intrinsic circadian clock is disrupted in human osteoarthritis.
Snelling SJ. et al, (2016), Chronobiol Int, 33, 574 - 579
In vitro effects of glutamate and N-methyl-D-aspartate receptor (NMDAR) antagonism on human tendon derived cells.
Dean BJ. et al, (2015), J Orthop Res, 33, 1515 - 1522
In vitro effects of glutamate and N-methyl- d -aspartate receptor (NMDAR) antagonism on human tendon derived cells
Dean BJF. et al, (2015), Journal of Orthopaedic Research, 33, 1515 - 1522
Differences in glutamate receptors and inflammatory cell numbers are associated with the resolution of pain in human rotator cuff tendinopathy.
Dean BJ. et al, (2015), Arthritis Res Ther, 17
Glucocorticoids induce senescence in primary human tenocytes by inhibition of sirtuin 1 and activation of the p53/p21 pathway: in vivo and in vitro evidence.
Poulsen RC. et al, (2014), Ann Rheum Dis, 73, 1405 - 1413
EPIGENETIC MODIFYING COMPOUNDS ALTER ACTIVITY OF PRIMARY HUMAN ARTICULAR CHONDROCYTES AND MESENCHYMAL STEM CELLS UNDERGOING CHONDROGENESIS
Snelling S. et al, (2014), OSTEOARTHRITIS AND CARTILAGE, 22, S141 - S141
A gene expression study of normal and damaged cartilage in anteromedial gonarthrosis, a phenotype of osteoarthritis.
Snelling S. et al, (2014), Osteoarthritis Cartilage, 22, 334 - 343
Epigenetic modifying compounds alter activity of primary human articular chondrocytes and mesenchymal stem cells undergoing chondrogenesis
Snelling SJB. et al, (2013), INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, 94, A16 - A16
Repairing damaged tendon and muscle: are mesenchymal stem cells and scaffolds the answer?
Davies BM. et al, (2013), Regen Med, 8, 613 - 630
THE ANATOMICAL SITE OF SYNOVIAL FLUID SAMPLING FROM THE OSTEOARTHRITIC KNEE: DOES IT MATTER?
Jayadev C. et al, (2013), OSTEOARTHRITIS AND CARTILAGE, 21, S74 - S74
SHORT-TERM SAMPLING STABILITY OF SYNOVIAL FLUID MEASUREMENTS IN KNEE OSTEOARTHRITIS
Jayadev C. et al, (2013), OSTEOARTHRITIS AND CARTILAGE, 21, S78 - S79
MULTIPLEX ANALYSIS OF OSTEOARTHRITIC SYNOVIAL FLUID: A COMPARISON OF LUMINEX & MESOSCALE DISCOVERY
Jayadev C. et al, (2013), OSTEOARTHRITIS AND CARTILAGE, 21, S73 - S73
HYALURONIDASE TREATMENT OF SYNOVIAL FLUID CAN IMPROVE MEASURED SIGNAL BY MULTIPLEX IMMUNOASSAY PLATFORMS
Jayadev C. et al, (2013), OSTEOARTHRITIS AND CARTILAGE, 21, S81 - S81
EPIGENETIC MODIFYING COMPOUNDS AFFECT THE ACTIVITY OF PRIMARY HUMAN ARTICULAR CHONDROCYTES AND MESENCHYMAL STEM CELLS UNDERGOING CHONDROGENESIS
Snelling S. et al, (2013), OSTEOARTHRITIS AND CARTILAGE, 21, S131 - S131
Aging mechanisms in arthritic disease.
Sacitharan PK. et al, (2012), Discov Med, 14, 345 - 352
DKK3 CAN PREVENT CARTILAGE DEGRADATION AND REGULATE CHONDROCYTE CELL SIGNALLING
Snelling S. et al, (2012), RHEUMATOLOGY, 51, 99 - 99
DKK3 CAN PREVENT CARTILAGE DEGRADATION AND MODULATE TGFBETA AND WNT SIGNALLING
Snelling S. et al, (2012), OSTEOARTHRITIS AND CARTILAGE, 20, S10 - S10
DICKKOPF-3 CAN REGULATE CARTILAGE DEGRADATION AND CHONDROCYTE CELL SIGNALLING
Snelling SJ. et al, (2011), OSTEOARTHRITIS AND CARTILAGE, 19, S119 - S119
Evidence for a role of Dickoppf-3 (Dkk3) in osteoarthritis
Snelling SJB. et al, (2011), INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, 92, A25 - A26
BMP5 activates multiple signaling pathways and promotes chondrogenic differentiation in the ATDC5 growth plate model.
Snelling SJ. et al, (2010), Growth Factors, 28, 268 - 279
Apoptosis in anteromedial gonarthrosis - evidence for the role of reactive oxygen species
Rout R. et al, (2010), INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, 91, A33 - A34
A gene expression profile of damaged vs. undamaged cartilage in anteromedial gonarthrosis
Rout R. et al, (2010), INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, 91, A35 - A35
The 2009 British Orthopaedic Research Society/Orthopaedic Research Society Travelling Fellowship
Khan WS. et al, (2009), JOURNAL OF BONE AND JOINT SURGERY-BRITISH VOLUME, 91B, 1537 - 1540
Osteoarthritis Research Society International - 12th annual meeting
Snelling S., (2008), IDRUGS, 11, 82 - 86
Osteoarthritis Research Society International--12th Annual Meeting. 6-9 December 2007, Fort Lauderdale, FL, USA.
Snelling S., (2008), IDrugs, 11, 82 - 86
Osteoarthritis genetics: current status and future prospects
Wilkins JM. et al, (2007), Future Rheumatology, 2, 607 - 620
An SNP in the 5'-UTR of GDF5 is associated with osteoarthritis susceptibility in Europeans and with in vivo differences in allelic expression in articular cartilage.
Southam L. et al, (2007), Hum Mol Genet, 16, 2226 - 2232
Genetic association analysis of LRCH1 as an osteoarthritis susceptibility locus.
Snelling S. et al, (2007), Rheumatology (Oxford), 46, 250 - 252
Allelic expression analysis suggests that cis-acting polymorphism of FRZB expression does not contribute to osteoarthritis susceptibility.
Snelling S. et al, (2007), Osteoarthritis Cartilage, 15, 90 - 92
The influence of tumour microenvironmental factors on the efficacy of cisplatin and novel platinum(IV) complexes.
Mellor HR. et al, (2005), Biochem Pharmacol, 70, 1137 - 1146
Comparison of TGFβ expression in healthy and diseased human tendon
Dakin SG. et al, Arthritis Research and Therapy

Key publications

A gene expression study of normal and damaged cartilage in anteromedial gonarthrosis, a phenotype of osteoarthritis.
Snelling S. et al, (2014), Osteoarthritis Cartilage, 22, 334 - 343
Presence of IL-17 in synovial fluid identifies a potential inflammatory osteoarthritic phenotype.
Snelling SJ. et al, (2017), PLoS One, 12
A comparative evaluation of the effect of polymer chemistry and fiber orientation on mesenchymal stem cell differentiation.
Rowland DC. et al, (2016), J Biomed Mater Res A, 104, 2843 - 2853
Dickkopf-3 is upregulated in osteoarthritis and has a chondroprotective role.
Snelling SJ. et al, (2016), Osteoarthritis Cartilage, 24, 883 - 891
H3K27me3 demethylases regulate in vitro chondrogenesis and chondrocyte activity in osteoarthritis.
Yapp C. et al, (2016), Arthritis Res Ther, 18

Recent Publications

Resorbable electrospun polydioxanone fibres modify the behaviour of cells from both healthy and diseased human tendons.
Kendal A. et al, (2017), Eur Cell Mater, 33, 169 - 182
Presence of IL-17 in synovial fluid identifies a potential inflammatory osteoarthritic phenotype.
Snelling SJ. et al, (2017), PLoS One, 12
Differential expression of alarmins-S100A9, IL-33, HMGB1 and HIF-1α in supraspinatus tendinopathy before and after treatment.
Mosca MJ. et al, (2017), BMJ Open Sport Exerc Med, 3
Identifying the optimum source of mesenchymal stem cells for use in knee surgery.
Davies BM. et al, (2016), J Orthop Res
Biocompatibility of implantable materials: An oxidative stress viewpoint.
Mouthuy PA. et al, (2016), Biomaterials, 109, 55 - 68

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