[cap30012]

I understand that choleterol are deposited in the blood vessel's walls by LDL, but what keeps them there? Isn't an end of cholesterol hydrophilic (though I believe there is another kind of cholesterol which is non-polar due to the chain of hydrocarbons connected to the hydroxyle group) ? Why would the cholesterol not be washed away by the largely water content blood? Also, do phospholipids wash away the cholesterol as they pass by in the blood, due to their polar heads and non-polar tails?

[GSR]

Hi,
 do you know abpout the foal cells and Atherosclerosis?.

the following information(from web) would clarify your doubt.

Atherosclerosis is the buildup of plaque on the inside walls of arteries. Plaque is made up of low density lipoprotein (LDL), macrophages, smooth muscle cells, platelets, and other substances. It may narrow the lumen of a blood vessel and restrict blood flow. Plaque rupture can induce the formation of thrombus (blood clot) and block blood flow. This will result in ischemic stroke or heart attack.

Formation of foam cells

The first stage in the development of atherosclerosis is the formation of foam cells (macrophages with ingested oxidized LDL). The process begins with trap of LDL in the intima, which lies just below the endothelium (the monolayer of cells lining the arterial wall). Trapped LDL could be oxidized, triggering recruitment of monocytes into the intima. Several adhesion molecules are involved, including vascular-cell adhesion molecule (VCAM), integrin, selectin, and others. After entering the intima, monocytes differentiate into macrophages and ingest oxidized LDL.

Formation of plaque

As atherosclerosis progresses, T lymphocytes, platelets and smooth muscle cells also join foam cells, expanding the plaque size. This involves cytokines to activate T lymphocytes and growth factors to promote proliferation of smooth muscle cells. Platelets can also release cytokines and growth factors to enhance migration and proliferation of smooth muscle cells. During this stage, a fibrous cap is formed to separate the plaque from the lumen.

Thrombosis

Thrombosis (formation of thrombus) arises from plaque rupture. Macrophages may release metalloproteinases and other proteolytic enzymes to degrade fibrous cap, making it susceptible to rupture. Plaque rupture activates platelets, leading to formation of  blood clots at the site of lesion .