Dear Amine, 

HDL are small, dense particles derived from the breakdown of the chylomicrons, and are composed of protein, cholesterol and phospholipid.  HDL have an important role transporting cholesterol from cells back to the liver. Plasma HDL is a powerful negative risk factor for atherosclerotic cardiovascular disease  as it has been found to promotes reverse transport of cholesterol from peripheral cells to the liver.  In addition, HDL protects LDL against oxidation, an effect mediated mainly by HDL associated enzymes such as paraoxonase, platelet activating factor acetylhydrolase (PAF-AH) and lecithin- cholesterol acyltranferase (L-CAT) (Schnell et al., 2001).  These enzymes have been shown to inhibit LDL oxidation in vitro and to convert bioactive lipid peroxidation products into inactive compounds. Oxidative modification of HDL results in deterioration in several biological functions critical to its role in reverse cholesterol transport (Schnell et al., 2001).  Sakai et al. (1992) found that oxidative modification of HDL impairs its binding to cells thereby reducing its effectiveness in promoting cellular lipid efflux.  Studies (Chait et al., 2004) have indicated that HDL is much more susceptible to oxidation than LDL. 

I hope that may help.

Best regards

Aly

Thesis Chapter 6-To investigate the antioxidant properties of dieta...

In my experience, HDL is taken up by cells (any cells) if they have HDL receptor SR-BI. Usually Apo AI and the size of the particle are the key factors in HDL uptake. 

Thank you both Aly and Sonika for replying

Yes Sonika, I agree with you, maybe SR-BI receptors could take up the HDL molecules by a LDLR-like mechanism, but this is not always the case, as sometimes there is just a transfer of lipids to hepatocytes predominantly by selective lipid uptake, via this receptor, without internalization of the particle. Plus, it's suggested that HDL catabolism is low (for more information you can read HDL endocytosis and resecretion (2013) authored by Röhrl et Stangl).

I had lately known that large cholesterol-ester rich HDL particles bind to SR-B1 with more affinity than small lipid poor HDL or lipid-free apo-AI. Maybe this will be the key of my question (ref. Scavenger receptor class B type I: a multifunctional receptor of Valacchi et al. 2011)