Apolipoprotein B
<p>Mar 2, 2008 10:33 PM
 
apo B is the primary apolipoprotein of LDL.
There is ONE apoB per particle (of VLDL, IDL, and LDL)
 
Apo B "unlocks the door to cells and thereby delivers cholest to them.
 </p>
<h2>Role in Lipoproteins and Atherosclerosis</h2>
<p>APOB100 is found in <a title="Lipoproteins" href="/wiki/Lipoproteins" class="mw-redirect">lipoproteins</a> originating from the liver (<a title="VLDL" href="/wiki/VLDL" class="mw-redirect">VLDL</a>, <a title="IDL" href="/wiki/IDL">IDL</a>, <a title="LDL" href="/wiki/LDL" class="mw-redirect">LDL</a>). Importantly, there is <b>one APOB100 molecule per hepatic-derived</b> lipoprotein. Hence, using that fact, one can quantify the <i>number</i> of lipoprotein particles by noting the total APOB100 concentration in the circulation. Since there is one and only one APOB100 per particle, the number of particles is reflected by the APOB100 concentration. The same technique can be applied to individual lipoprotein classes (e.g. LDL) and thereby enable one to <i>count</i> them as well.
It is well established that APOB100 levels are associated with <a title="Coronary heart disease" href="/wiki/Coronary_heart_disease">coronary heart disease</a>, and are even a better predictor of it than is LDL level. A naive way of explaining this observation is to use the idea that APOB100 reflects lipoprotein particle number (independent of their cholesterol content). In this way, one can infer that the number of APOB100-containing lipoprotein particles is a determinant of <a title="Atherosclerosis" href="/wiki/Atherosclerosis">atherosclerosis</a> and heart disease.
One way to explain the above is to consider that large numbers of lipoprotein particles, and, in particular large numbers of LDL particles, lead to competetion at the APOB100 receptor (i.e. LDL receptor) of peripheral cells. Since such a competition will prolong the residence time of LDL particles in the circulation, it may lead to greater opportunity for them to undergo <a title="Oxidation" href="/wiki/Oxidation" class="mw-redirect">oxidation</a> and/or other chemical modifications. Such modifications may lessen the particles' ability to be cleared by the classic LDL receptor and/or increase their ability to interact with so-called "scavenger" receptors. The net result is shunting of LDL particles to these scavenger receptors. Scavenger receptors typically are found on <a title="Macrophages" href="/wiki/Macrophages" class="mw-redirect">macrophages</a>, with cholesterol laden macrophages being better know as "<a title="Foam cells" href="/wiki/Foam_cells">foam cells</a>". Foam cells characterize atherosclerotic lesions. In addition to this possible mechanism of foam cell generation, an increase in the levels of chemically modified LDL particles may also lead to an increase in <a title="Endothelial" href="/wiki/Endothelial" class="mw-redirect">endothelial</a> damage. This occurs as a result of modified-LDL's toxic effect on vascular <a title="Endothelium" href="/wiki/Endothelium">endothelium</a> as well its ability both to recruit immune effector cells and to promote <a title="Platelet" href="/wiki/Platelet">platelet</a> activation.</p>