Transcriptional profiling of atherosclerotic disease (human and mouse)

It has been known for some time that atherosclerotic heart disease has a significant genetic component. Epidemiological studies have demonstrated familial aggregation of CAD and several of its risk factors. A family history of heart disease is also known to be an independent risk factor for atherosclerosis. In addition, twin studies suggest that 50% of the variation in atherosclerosis disease severity can be explained by genetic factors. However, despite this mounting evidence supporting the role of genetic factors in the etiology of atherosclerotic heart disease, little is known about the genes themselves. Association studies have shown that variants of several genes can increase the risk of myocardial infarction, but no gene has yet been identified in a large scale association study that adds to current risk markers, refines diagnosis or targets therapy in individual patients.
In the Quertermous lab we use transcription profiling as a tool to identify important genes relevant to atherosclerosis. Human tissue from explanted hearts or atherectomy specimens provides a rich resource of starting material, together with tissue from mouse models (which allows us to study disease in evolution). Our platform is currently a custom cDNA array (see Ho's publication) which will shortly give way to an oligonucleotide chip, developed in collaboration with Agilent technologies. Output from these experiments is analyzed using statistical tools and software developed at Stanford, Agilent, or here in the Q lab.

Other Research Areas:

- Overview
- Athero
  disease
- Endothelial
  cells
- Smooth
  muscle
  cells
- Cell
  remodeling
- Apelin
- Gene
  Hunting
- SAPPHIRe
- Heart 
  developing

People involed in this project:

- Euan
- Jenn
- Ray
- Roger
- Mary
- Alicia
- Josh