PhD in Biochemistry                                   

• University of Nottingham: Oct 1996-Aug 1999

Post Graduate Certificate in Education (PGCE)

• University of Nottingham: Sep 1994-Jul 1995

BSc. (Hons) Biochemistry & Biological Chemistry

•  University of Nottingham: Sep 1991-Jul 1994

Simon graduated from the University of Nottingham in 1994 with a BSc (Hons) in Biochemistry and Biological Chemistry. After undertaking a PGCE in Secondary School Education, he completed a PhD in 1999 where he investigated the fibre type specific expression and functional role of calpain proteases in skeletal muscle growth. He then spent 4 years as a Postdoctoral Research Fellow in the research group of Professor Paul Greenhaff (University of Nottigham) investigating the functional effect and molecular mechanisms of immobilisation-induced skeletal muscle atrophy and exercise rehabilitation, where he was the first to publish the effect of immobilisation in humans on the expression of muscle-specific ubiqitin ligases.

In 2003, Simon joined the Respiratory and Inflammation Research Area (RIRA) at AstraZeneca (Alderley Park) as a Senior Research Scientist. Here he investigated the utility of cell penetrating peptides (CPPs) for the cellular delivery of oligonucletide antisense and peptide cargo for the purpose of target validation studies (British Journal of Pharmacology, 2005).

Alongside this, he took a leading position within AstraZeneca's osteoarthritis (OA) drug discovery team by leading drug target identification and validation studies. Here he was successful in progressing the drug targets CXCR7/RDC1 and MAPKAPK2 (MK2) through to lead generation by demontrating their involvement in cartilage degeneration and chondrocyte hypertrophy (Osteoarthritis and Cartilage, 2006; Osteoarthritis and Cartilage 17, 2009). During this time he also made an important contribution to the field of non-coding RNAs, being the first to report the expression profile of microRNAs (miRNAs) in human OA cartilage and bone and to demonstrate that inhibition of specific miRNAs modulated MMP13 and TNFα production (Osteoarthritis and Cartilage, 2009).

In 2011, Simon took up the position of Research Laboratory Head at Boehringer-Ingelheim (Vienna, Austria), where he directed studies to validate new biological entities (NBEs) in oncology, including bi-paratopic antibody based drugs. 

In 2012 he transitioned from the pharmaceutical industry to take up the position of Senior Lecturer at the Institute of Inflammation and Ageing, University of Birmingham, where he established the Osteoarthritis and Musculoskeletal Inflammation Group and where he has been Chief Investigator on 5 NIHR-adopted clinical studies involving over 1000 patient participants. 

As principal investigator, Simon has secured over £2million in research funding from charities (including Versus Arthritis, Dunhill Medical Trust, Birmingham Orthopaedic Charity), UKRI (MRC, Wellcome Trust), and from Industry (AstraZeneca/MedImmune, Nuvasive, Eli Lilly).

His research group was the first to report on the role of long non-coding RNAs (lncRNAs) in the inflammatory response of human OA chondrocytes (Arthritis Rheumatology. 68(4):845-56, 2016), and more recently on the functional role of the lncRNA MALAT1 in mediating the inflammatory synovial fibroblast phenotype (Arthritis Rheumatology, 2020).

His current research, supported by funding from the MRC Advanced Pain Discovery Platform (APDP) and Eli Lilly Global Pain Discovery, involves leading a consortium of researchers to investigate the role of pain-associated fibroblast subsets (EBioMedicine, 2022) in mediating inflammatory OA joint pain.

Simon was promoted to Reader in 2019, and in 2022 to Professor in Musculoskeletal Ageing.

Prof Jones’ research group conducts clinical translational research studies to investigate the inflammatory and metabolic mechanisms that drive musculoskeletal ageing disorders including osteoarthritis (OA) and sarcopenia.

A particular area of research interest is the functional role of non-coding RNAs in mediating inflammatory responses, and the impact of obesity in mediating chronic inflammation and ageing.

He is Chief Investigator on five NIHR-adopted clinical studies involving OA patients, through which he has established a biobank of tissues and derived primary cells (chondrocytes, myoblasts, synovial fibroblasts and osteoblasts) from over 1000 well-characterised patient cohorts.

He was the first to report on the role of the novel long non-coding RNA (lncRNA) family in the inflammatory response of human OA chondrocytes (Arthritis Rheumatology. 68(4):845-56, 2016), and on the functional role of the lncRNA MALAT1 in mediating the inflammatory obese OA synovial fibroblast phenotype (Arthritis Rheumatology, 72 (4), 609-619, 2020). Importantly, showing that targeted inhibition of MALAT1 in the joint could be a therapeutic approach to reducing synovial joint inflammation in obese OA patients.

More recently, following a 4-year clinical study, his group reported that synovial tissue at sites of joint pain in OA patients exhibits a differential phenotype with distinct synovial fibroblast subsets (EBioMedicine, 72, 103618, 2021).