If you want someone with serious expertise on the separation of plasma lipids using an ultracentrifuge then Krauss, obviously, is your man. Author number nine out of twelve on this next paper. He was, obviously, their man too.
If you want to look at oxidised lipids in lipoproteins you need an antibody which locks on to oxidised lipids but not to undamaged lipids. This is called E06. It is quite specific and only binds to the phosphocholine residue of an oxidised phospholpid. It's probably the most commonly used antibody for detecting oxLDL. Or what people thought was oxLDL until this paper came out.
What did this group do? All sorts of things, most of them very clever in deed.
Let's scream through the results. First they took an antibody to Lp(a) and pulled the Lp(a) out of plasma with it. E06 reactivity was pulled out along side Lp(a).
They got Krauss to spin some lipids and found, lo and behold, E06 reactivity separated out ONLY with the Lp(a) fraction.
They took some LDL and oxidised it artificially with copper ions. Then they offered it a choice of Lp(a) or native LDL to share lipids with. Not only did E06 reactivity jump out of the oxLDL and in to Lp(a), it ONLY jumped in to the Lp(a). None jumped from copper oxidised LDL to native LDL. None would leave its Lp(a), even to go to another Lp(a).
They went on to check if Lp(a) is just susceptible to oxidation in its own right, by looking for malondialdehyde-lysine residues. It's not oxidised itself. It just collects oxidised lipids. The antibody for malondialdehyde-lysine is E14. It ignores Lp(a). However the E06 antibody to oxidised phospholipid not only recognised Lp(a) but also apo(a) alone, presumably both from sources where they have had access to oxidised lipids.
The implication from this is that while some of the oxidised phospholipids are in the lipid particle of the Lp(a), a big chunk are also bound to the apo(a) protein.
The group feel that apo(a) initially captures oxidised phospholipids from the aqueous plasma phase and they are then transfer over several hours to the lipid droplet.
EDIT: I miss read this, the lipid drop captures the oxidised phospholipds and then they get arranged on the apo(a) glycoprotein. This may have some relevance to apo(a) isoforms, Lp(a) levels and vascular injury.
They doubt that Lp(a) really goes around stealing oxidised lipids from oxLDL particles. What they suspect is happening is that whenever oxidised lipids are released from damaged tissues, Lp(a) is the mop which mops them up. They probably never get as far as native LDL.
As far as they are concerned Lp(a) IS oxLDL. And oxLDL IS Lp(a).
Do tissue damage, the liver makes a sponge for oxidised tissue lipids. Probably many more oxidised lipids than E06 recognises.
You have to wonder whether the liver senses free oxidised lipids in the bloodstream and makes apo(a) in response to them (almost certainly the case, because Lp(a) spikes after injuries such as percutaneous cardiac procedures, where everyone expects oxidised lipids to be mechanically released without dietary warning). Or whether, as in the Finland intervention, volunteers do something grossly stupid such as reducing the fat content of their diet. And the liver pre-empts...
Probably a bit of both.
So, Beth, you asked in the comments section of the last Lp(a) post:
What does Lp(a) actually do?
It preferentially accumulates oxidised lipids and binds them in a form where they cannot be immediately excreted from the plasma. It also puts a great big sticky label on them that allows them to firmly bind to damaged tissue.
Only Lp(a) does this.
Only in humans and related apes. Oh, and in mice genetically engineered with both human apoB100 and apo(a) in combination. Of course.
That too is an interesting question.