Grants and Contracts Details
Serum amyloid A, along with high sensitivity C] Reactive Protein, is a clinical marker of atherosclerosis, a vascular inflammatory disease responsible for half a million deaths per year in the US. Interestingly, SAA is modestly but chronically elevated in several diseases such as diabetes and obesity that confer greater risk to developing atherosclerosis. Thus SAA may play a causal role in atherosclerosis development. We and others have demonstrated that increased SAA in mice accelerates atherosclerosis. The focus of this proposal is to test the mechanism by which SAA increases the development of atherosclerosis. As outlined in the response to retention hypothesis of atherosclerosis, proteoglycan mediated lipoprotein retention is thought to be a key initiating step. Our preliminary data shows that mice overexpressing SAA have increased biglycan in their vessel wall and an increase in atherosclerosis. SAA, an apoprotein, also possesses a proteoglycan binding domain and thus could mediate an interaction between the vascular matrix and lipoproteins. This research proposal will determine if biglycan is required to retain proatherogenic lipoproteins after SAA stimulation and will determine if SAA acts as a bridging molecule to enhance proteoglycan]lipoprotein interaction as mechanism to explain the increased atherosclerosis observed.
|Effective start/end date||7/1/12 → 6/30/14|
- American Heart Association Great Rivers Affiliate: $50,000.00
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