Applied Maths Seminar: Watson -- Mathematical models for cell and lipid dynamics in atherosclerotic plaques

Mike Watson (UNSW) is currently on sabbatical in the department, and will give a seminar
on Wednesday 17th September at 1pm in Carslaw 275.  We will go to lunch with the speaker
beforehand, leaving Carslaw Level 2 at 12.05pm promptly.  Lunch is free for students.  

Title: Mathematical models for cell and lipid dynamics in atherosclerotic plaques 

Abstract: Atherosclerotic plaques are fatty, cellular lesions that form in artery walls
and can lead to heart attack or stroke.  Plaques are initiated by blood-borne lipid
particles ("bad cholesterol") that become trapped in the artery wall and trigger an
immune reaction.  Subsequent plaque progression involves a complex interplay between
these lipids and the cells that are recruited to the lesion site.  

The two main cell types in plaques are macrophages and smooth muscle cells.  Macrophages
are specialised immune cells that are recruited to the early plaque to ingest and remove
retained lipids.  Smooth muscle cells (SMCs) are artery wall-resident cells that are
recruited to the plaque when ineffective lipid removal by macrophages leads to the
localised accumulation of lipid and dead cells.  SMCs form a protective cap over this
hazardous material but can also undergo a harmful transition towards a defective
macrophage-like phenotype.  

In this talk, I will discuss two different models for the cell and lipid dynamics in
plaques.  The first is a reaction-diffusion type model of macrophage migration and lipid
ingestion in the early plaque.  We consider how the capacity of macrophages to remove
lipid by emigration influences the trajectory of the early plaque and shapes its early
spatial structure.  The second model proposes a system of ODEs to study SMC phenotype
transition in the mid-stage plaque.  We consider how the exposure of cap SMCs to
uncleared lipid can drive this transition and accelerate plaque progression.  These two
models represent a small part of a larger body of recent modelling research that aims to
provide novel mechanistic insight into the formation of dangerous atherosclerotic
plaques.