Biosapien, like everyone else who has seen that presentation, I found it quite interesting.
I'm curious as to whether you have an opinion on whether that process is the one that occurs in monocytes that stick to arterial endothelium as the first stage of development of atheromas. I'll describe the process.
As far back as 1981,
Gerrity published the results of experimental reproduction of atheromatosis in pigs here --https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1903817/pdf/amjpathol00218-0023.pdf. The author mentioned a previous experiment in which he and his colleagues fed an atherogenic (causing atheromas to form) diet to pigs (lard and cholesterol) and demonstrated that atheroma development was preceded by white blood cells of the type called a monocyte, penetrating the layer of cells that line the aorta. In this experiment, they found these monocytes in various locations of the endothelial lining layer of arteries --1) sticking to the surface of the cells lining the arteries, as well as 2) in the junction between the cells that line arteries, and also 3) inside the inner wall of the arteries. In addition, the examination suggested that the monocytes were differentiating (changing) into macrophages (cells that gobble up debris) before becoming foam cells. Ferritin was injected into the arteries and found to be taken up by those monocytes that had penetrated between the cells lining the arteries. This indicates that the monocytes were becoming scavengers of debris even before they had changed into macrophages.
Bobryshev (2006;
https://www.sciencedirect.com/science/a ... 2805001642) gave a more up-to-date review. He affirmed that monocytes migrate into the tissue under the cells lining arteries (endothelium), differentiate into macrophages and dendritic cells before differentiating again into foam cells. The author went on to claim that these cells aggregate to form a core that consists of a necrotic plaques, lipids, cholesterol crystals and cell debris.
Bobryshev also mentioned the presence of a number of chemicals associated with inflammation in these atheromatous lesions. Inflammation accompanies atheroma formation.
I've inserted a diagram of my simplistic interpretation of the process at the end of this thread.
Apparently Activated Protein C (a Vitamin K-dependent Protein) has the capacity to neutralise these vascular adhesion molecules -- Activated Protein C (APC) and Protein S have been shown to also play a role in the health and permeability of vascular endothelium. Wikipedia has an excellent review of the role of Protein C on this website -
https://en.wikipedia.org/wiki/Protein_C ... seegers-10 . This Wikipedia review describes how APC has anti-inflammatory effects on endothelial cells and leukocytes. APC protects endothelial cells by inhibiting inflammatory mediator release and by
down-regulating vascular adhesion molecules. This tends to negate the initial process of monocytes sticking to the endothelial cells, and infiltrating into, while also limiting damage to, underlying tissue. APC supports endothelial barrier function and reduces the effects of the chemicals that attract monocytes into the tissues under the endothelium. In effect, it negates every untoward biochemical process involved in the formation of atheromas.
I would appreciate your comments.