PhD Research Studentships
Effect of blood sugar on cartilage inflammatory joint disease post menopause
| Supervisors: | Martin KNIGHT, Timothy HOPKINS and Josephine WU |
| Apply by: | 28 January 2026 |
| Start in: | September (Semester 1) |
Description
Osteoarthritis (OA) is the most common joint disease in the world, affecting over 500 million people and representing a significant economic and societal burden. Joint inflammation is a common feature of OA; a vicious cycle resulting in and from the production of inflammatory cytokines, which stimulate catabolic signalling pathways. The result is cartilage degradation and subchondral bone remodelling, ultimately leading to loss of joint function. Given the greater prevalence of OA in post-menopausal females, there is increasing interest in the role of reduced oestrogen in the onset and pathogenesis of OA. It has been suggested that this relationship is mediated metabolically; a reduction in oestrogen can result in insulin resistance, leading to poor glucose regulation, which is thought to be a driver of joint inflammation. This is compounded by high glucose diets, the pervasiveness of which is increasing globally. Thus, there is increasing interest in how the levels of blood sugars and insulin effect joint inflammation and the efficacy of anti-inflammatories.
This PhD project will develop organ-on-a-chip models to examine the direct effect of blood sugars, insulin and oestrogen levels on the response of cartilage and subchondral bone to pro-inflammatory signalling, which drives degradation in arthritis. Initial studies will be conducted with isolated human chondrocytes. This will lead on to a more comprehensive organ-chip models involving a vascularised osteochondral tissue created within commercial microfluidic platforms available within the Centre (Emulate or Mimetas). These bone-cartilage models will be generated using growth factors to spatially control osteogenic and chondrogenic differentiation of human mesenchymal stem cells, as in recent studies from the supervisors (Hopkins T et al. Journal of Tissue Engineering 2024). The efficacy of anti-inflammatories in response to changes in glucose and insulin will be tested within the in vitro models helping to inform guidance on therapeutic usage.
The project will also examine underlying fundamental mechanisms associated with changes in chondrocyte primary cilia which have been reported to occur in response to insulin and glucose. Whilst primary cilia have been shown to regulate insulin secretion, pioneering studies by Knight’s group have shown that primary cilia and associated intraflagellar transport are also involved in pro-inflammatory signaling in a variety of cell types. Unravelling the mechanistic effect may help to develop new strategies for managing inflammatory joint disease.
Funding
Funded by: China Scholarship CouncilCandidate will need to secure a CSC scholarship.
Under the scheme, Queen Mary will provide scholarships to cover all tuition fees, whilst the CSC will provide living expenses and one return flight ticket to successful applicants.
Eligibility
- The minimum requirement for this studentship opportunity is a good honours degree (minimum 2(i) honours or equivalent) or MSc/MRes in a relevant discipline.
- If English is not your first language, you will require a valid English certificate equivalent to IELTS 6.5+ overall with a minimum score of minimum score of 6.0 in each of Writing, Listening, Reading and Speaking).
- Candidates are expected to start in September (Semester 1).
Contact
For informal enquiries about this opportunity, please contact Martin KNIGHT, Timothy HOPKINS or Josephine WU.
Apply
Start an application for this studentship and for entry onto the PhD FT Medical Engineering full-time programme (Semester 1 / September start):
Please be sure to quote the reference "SEMS-PHD-705" to associate your application with this studentship opportunity.
| Keywords: | Genetic Engineering, Bioengineering, Biomedical Engineering, Tissue Engineering |