Endocytosis, Familial Hypercholesterolemia, and Atherosclerosis

Campbell Biology

LDL receptors of normal cell take in cholesterol for synthesis. Cell without LDL receptors leave cholesterol in the blood which contributes to atherosclerosis.
Source: Urry, Lisa A.. Campbell Biology (p. 139). Pearson Education. Kindle Edition.

In endocytosis, the cell takes in molecules and particulate matter by forming new vesicles from the plasma membrane. Although the proteins involved in the processes are different, the events of endocytosis look like the reverse of exocytosis. First, a small area of the plasma membrane sinks inward to form a pocket. Then, as the pocket deepens, it pinches in, forming a vesicle containing material that had been outside the cell. Human cells use receptor-mediated endocytosis to take in cholesterol for membrane synthesis and the synthesis of other steroids. Cholesterol travels in the blood in particles called low-density lipoproteins (LDLs), each a complex of lipids and a protein. LDLs bind to LDL receptors on plasma membranes and then enter the cells by endocytosis. In the inherited disease familial hypercholesterolemia, characterized by a very high level of cholesterol in the blood, LDLs cannot enter cells because the LDL receptor proteins are defective or missing.

Consequently, cholesterol accumulates in the blood, where it contributes to early atherosclerosis, the buildup of lipid deposits within the walls of blood vessels. This buildup narrows the space in the vessels and impedes blood flow, potentially resulting in heart damage and stroke.

Endocytosis and exocytosis also provide mechanisms for rejuvenating or remodeling the plasma membrane. These processes occur continually in most eukaryotic cells, yet the amount of plasma membrane in a nongrowing cell remains fairly constant. The addition of membrane by one process appears to offset the loss of membrane by the other.

Source:

Urry, Lisa A.. Campbell Biology (p. 139). Pearson Education. Kindle Edition.

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