Cholesterol does not cause atherosclerosis. Oxidized cholesterol byproducts do.

Here are a few things to keep in mind:  1) Cholesterol is not soluble in water or blood.  A derivative of cholesterol that is soluble in blood or water is not cholesterol.  2) The only way cholesterol is moved around either in the blood or as an adduct is by the action of adding a hydrophilic protein or converting free cholesterol enzymatically to a soluble form.  3) The only way cholesterol gets to an artery wall is through a lipoprotein or the soluble form made first by a cell's action upon ingested cholesterol.  4) It has already been proven that native LDL is harmless to endothelial layers even in very high concentrations of the particle and that the oxLDL particle is the one that causes havoc to the endothelial layer.

That being said, even in the most severely diseased coronary artery disease (CAD) patient with acute coronary syndrome (ACS) presenting as angina, respiratory problems, and/or MI, the level of oxLDL is 4-5mg/dL maximally.  Normally, they are half this value to none.  This value of 4-5 doesn't occur until after the coronary artery disease, so how could it be that oxLDL caused the CAD?  Temporally, and logically, oxLDL could not have caused CAD if it was absent beforehand.

There is no question that toxic adducts of cholesterol DO cause arteriosclerosis and the consequence is atherosclerosis.  Is it an inevitable event that cholesterol becomes 25-hydroxycholesterol and cholestane-3beta, 5alpha, 6beta-triol, the culprits of endothelial aggravation?  No.

It is not cholesterol, it is OXIDATION that causes these culprit oxidized cholesterol molecules to arise and cause harm.  By having administered pure non-oxidized cholesterol to the artery cells with no harm, scientists made sure of the fact as early as 1976.  Extending the first post, here are younger studies confirming the first.

Effect of auto-oxidation products from cholesterol on aortic smooth muscle cells: an in vitro study.

Cytotoxicity of oxidation derivatives of cholesterol on cultured aortic smooth muscle cells and their effect on cholesterol biosynthesis.

Ironically, the hydroxycholesterol and other oxygen adducts shut off cellular cholesterol synthesis, making the matter worse as your cells, especially the fastest dividing ones, make it for a mission critical reason.  As the repeat, "Purified cholesterol showed no cytotoxic effect and minimal inhibition of cholesterol biosynthesis"

Inhibitory effect of cholesterol oxides on low density lipoprotein receptor gene expression.

Again, after two decades, the groups repeat that ". Pure cholesterol showed only minimal inhibition."

The question of importance is how much of the toxic oxygenated cholesterol is there in food?  Who would know for something boiling around in hot oil and open air for weeks?  My guess is a significant amount of cholesterol has turned to ox-cholesterol and probably stuff like that should be avoided.  Minimally cooked foods, or fresh foods would have a minimum of this toxic cholesterol derivative.  So indeed, the way meat is cooked may be a significant way to introduce these cholesterol-oxygen problem compounds in the blood, and these are indeed soluble.
 
However, like most everything, there is a reason for this artery aggravating 25-hydroxycholesterol (immune response against viruses) to exist:

Armand-Frappier Outstanding Student Award--The emerging role of 25-hydroxycholesterol in innate immunity.

25-Hydroxycholesterols in innate and adaptive immunity.

There is an enzyme that responds to interferon by hydroxylating cholesterol.  25HC is antiviral.

Given that your blood levels of ApoB bound cholesterol are from your liver and not from a vat of oil boiling around for weeks, it would not cause any arterial injury.  This is dependent on antioxidant functions preventing oxidation.  These are enzymatic, such as PON and glutathione, and enteral/parenteral such as Vitamin C, E, and A.