A key early event in atherosclerosis is the retention of LDL by proteoglycans chains in the artery wall. This is followed by a chronic inflammatory process ultimately leading to the formation of atherosclerotic plaques. The aim of this work is to prevent the atherogenic changes on the chains of proteoglycans. Recently meta-analysis have concluded that periodontal disease and CVD are significantly related. Hence this project will seek to explore the mechanisms and describe the pathway relating oral infection to atherosclerosis.

Recently we have data showing that LPS via TLR-4 stimulates the mRNA expression of the rate limiting genes involved in the elongation of GAG chains on proteoglycans. TLRs have multiple downstream signalling pathways so we will determine which of the possible signalling pathways is linked to the expression of genes for GAG enzymes (and this a potential therapeutic target). For this project we will utilise LPS-PG a purified preparation of lipopolysaccharide (LPS) from the Gram-negative bacteria Porphyromonas gingivalis. LPS-PG is an important virulence factor in the mechanisms of periodontal disease.

Expected outcomes and deliverables:

This is a wet lab based project the student will gain experience in cell culture, biochemistry, experimental design, data analysis and presentation skills. The data collected by the student will be used to generate a publication.

Suitable for:

This project is opened for students who have completed some practical classes during undergraduate studies. This project would suit students with pharmacology/biomedical interests or related discipline.

Project members

Dr Danielle Kamato

Honorary Research Fellow
School of Pharmacy

Emeritus Professor Peter Little

Emeritus Professor
School of Pharmacy