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Staff Profile

Professor David Young

Professor of Musculoskeletal Biology

  • Telephone: +44 (0) 191 241 8831
  • Personal Website: https://blogs.ncl.ac.uk/davidyoung/
  • Address: Skeletal Research Group
    Regenerative Medicine, Stem Cells and Transplantation Theme
    Biosciences Institute
    Newcastle University
    Central Parkway
    Newcastle upon Tyne
    NE1 3BZ
Background

Current

My group are members of the Regenerative Medicine, Stem Cells and Transplantation Theme, Biosciences Institute, Newcastle University. Twitter:@IGM_YoungLab 

Qualifications

BSc, University of Sheffield, 1989-1992
PhD, Cambridge laboratory, John Innes Centre, Norwich (UEA affiliated), 1992-1996

Previous Positions

1997-1998. ARC Post-doctoral Research Assistant, Wellcome Trust Centre for Matrix Research, University of Manchester.
1998-2003. ARC Senior Post-doctoral Research Assistant, School of Biological Sciences, University of East Anglia.
2003-2004. Dunhill Medical Trust Post-doctoral Research Assistant, School of Biological Sciences, University of East Anglia.

Memberships

Member of the Biochemical Society
Previously honorary treasurer and committee member of the British Society for Matrix Biology (BSMB)


Areas of expertise

  • Cartilage biology
  • Osteoarthritis
  • Epigenetics
  • MicroRNA

Google scholar: Click here.
ORCID: Click here.



Research

Research Interests

We are members of the Regenerative Medicine, Stem Cells and Transplantation Theme.

My research interests include gene expression and regulation in the context of cartilage development and the main cartilage disease, osteoarthritis (OA). My laboratory focus is how these genes are epigenetically regulated; by microRNAs, DNA methylation and chromatin modifications.

Other Expertise

Main techniques: Gene expression analysis/profiling (Real-time PCR, microarray, RNA-seq). Cell signalling analysis. RNAi (siRNA, shRNA). miRNA analysis. Cas9/CRISPR. ChIP-seq, ATAC-seq. Transcription factor analysis (EMSA, mutagenesis, reporter assays). Epigenetic analysis. Models of osteoarthritis.

Current Work

Age is the major risk factor for Osteoarthritis. We are investigating the molecular mechanisms of how ageing impacts on cartilage.

Manipulating gene expression in cartilage is currently not possible therefore we have developed an interest in tissue engineering, to generate cartilage from the differentiation of stem cells. Using this model we have generated a series of -omics scale data to help understand what controls a chondrocyte phenotype.

We are developing CRISPR technology in the group both in terms of their ability to edit genes and also to regulate transcription. With collaborators we are using CRISPR to generate novel transgenics.



Post-doctoral Scientists

Clinical trainee fellow

  • Adam Farrier

Past Lab members

  • Jamie Soul
  • Yao Hao
  • Dan Hayman
  • Hua Lin
  • David Wilkinson
  • Adrian Falconer
  • Marta Radwan
  • Siliva Lecci
  • Bola Ajekigbe
  • Dimitra Tsompani
  • Heather Bromby
  • Steven Woods
  • Rodolfo Gomez
  • Katie Crossland
  • Wang Hui
  • Yaobo Xu
  • Catherine Bui
  • Christos Gavriilidis
  • Jenny Scott
  • Hannah Elliott
  • Martin Galler


Esteem Indicators

Previously British Society for Matrix Biology (BSMB) Honorary Treasurer

http://www.bsmb.ac.uk

Funding

Current funding is mainly from the Dunhill Medical Trust, the JGW Patterson Foundation, Versus Arthritis, Newcastle NHS Hospital Charity, and CIMA (MRC/Arthritis Research UK).

Industrial Relevance

More than 7 million adults in the UK (15% of the population) have long-term health problems due to arthritis and related conditions. In 2001 incapacity benefit alone cost the nation £2.4 billion.

Metalloproteinases are the enzymes ultimately responsible for the collagen loss to cartilage seen in arthritic diseases. The design of small molecule inhibitors of the metalloproteinases remains a major focus of the pharmaceutical industry, yet has been largely unsuccessful, probably due to a lack of specificity of the compounds and side effects. Since arthritis is a debilitating, but not fatal disease, such side effects need to be minimised. We suggest that HDACi will be chondroprotective in all destructive arthritides, including both rheumatoid arthritis and osteoarthritis (other examples include: reactive arthritis, gout/pseudogout, psoriatic arthritis). They may also show utility in cartilage engineering/transplantation to protect cartilage explants or engineered/cultured cartilage from degradation. Many pharmaceutical companies are currently testing HDACi in cancer therapy trials, therefore these molecules potentially represent the next wave of drugs to fight the arthiitis.

Teaching


I regularly supervise Masters of Research and undergraduate students for laboratory projects.


I teach on the Masters of Research Biology of Ageing (MMB8011) and Tissue Engineering (MEC8060).


I am Programme and module leader for Regenerative Medicine and Stem Cells (MMB8022).


I was previously DPD for MRes projects (MMB8099).

Publications