User:Ian Kates
My name is Ian Kates and I am an undergraduate student at Boston College. The purpose of my account and any activity that I may partake in on Wikipedia is to further the knowledge and information of neuroscience on Wikipedia.
Introduction to Neuroscience
[edit]A Class Project
[edit]I am currently taking a course called BI481 Introduction to Neuroscience. As a part of the course, we are have been tasked with helping the Society for Neuroscience expand the field of neuroscience in Wikipedia. Any changes that me or my group makes in Wikipedia will be due to our class project.
Links to the project proposal and the VLDL receptor page can be found below.
VLDL Receptor Project Proposal
Atherosclerosis
[edit]A pathological hallmark of atherosclerotic cardiovascular disease is the excessive accumulation of cholesterol by macrophages, leading to their transformation into foam cells. Accululation of cholesterol is caused by dysregulation of of the balance of cholesterol infulx and efflux. Foam cell accumulation initiates early atherosclerotic lesions in the arteries. Macrophages absorb cholesterol through many pathways and receptors. In addition, macrophages also express scavenger receptors, which internalize oxidatively modified lipoproteins. VLDL receptor has been identified as a receptor expressed by macrophages.[1]
Experiments showed that diet-induced atherosclerosis was facilitated by the LDL receptor. It is also a major pathway for the uptake of VLDL by the macrophage. In addition, the experiments showed that the VLDL receptors did not respond to cholesterol loading due to diet. To test the role of VLDL receptors, VLDL receptor expression was reconsitituted into mice with a VLDL receptor knockout. Reconstitution of VLDL receptor expression greatly increased atherosclerotic lesion development. The result of these experiments have implicated macrophage VLDLR is a pro-atherogenic factor..[2]